Ada2011

Standards of Medical Care in Diabetes—2011AMERICAN DIABETES ASSOCIATION

CONTENTS

I. CLASSIFICATION AND DIAGNOSISOF DIABETES, p. S12

A. Classification of diabetesB. Diagnosis of diabetesC. Categories of increased risk for di-

abetes (prediabetes)II. TESTING FOR DIABETES IN ASYMP-

TOMATIC PATIENTS, p. S13A. Testing for type 2 diabetes and risk

of future diabetes in adultsB. Testing for type 2 diabetes in chil-

drenC. Screening for type 1 diabetes

III. DETECTION AND DIAGNOSIS OFGESTATIONAL DIABETES MELLI-TUS, p. S15

IV. PREVENTION/DELAY OF TYPE 2DIABETES, p. S16

V. DIABETES CARE, p. S16A. Initial evaluationB. ManagementC. Glycemic control

1. Assessment of glycemic controla. Glucose monitoringb. A1C

2. Glycemic goals in adultsD. Pharmacologic and overall ap-

proaches to treatment1. Therapy for type 1 diabetes2. Therapy for type 2 diabetes

E. Diabetes self-management educa-tion

F. Medical nutrition therapyG. Physical activityH. Psychosocial assessment and careI. When treatment goals are not metJ. HypoglycemiaK. Intercurrent illnessL. Bariatric surgeryM. Immunization

VI. PREVENTION AND MANAGEMENTOF DIABETES COMPLICATIONS, p.S27A. Cardiovascular disease

1. Hypertension/blood pressurecontrol

2. Dyslipidemia/lipid management3. Antiplatelet agents4. Smoking cessation5. Coronary heart disease screen-

ing and treatmentB. Nephropathy screening and treat-

mentC. Retinopathy screening and treat-

mentD. Neuropathy screening and treat-

mentE. Foot care

VII. DIABETES CARE IN SPECIFIC POP-ULATIONS, p. S38A. Children and adolescents

1. Type 1 diabetesGlycemic controla. Screening and management of

chronic complications in chil-dren and adolescents withtype 1 diabetesi. Nephropathyii. Hypertensioniii. Dyslipidemiaiv. Retinopathyv. Celiac diseasevi. Hypothyroidism

b. Self-managementc. School and day cared. Transition from pediatric to

adult care2. Type 2 diabetes3. Monogenic diabetes syndromes

B. Preconception careC. Older adultsD. Cystic fibrosis–related diabetes

VIII. DIABETES CARE IN SPECIFICSETTINGS, p. S43

A. Diabetes care in the hospital1. Glycemic targets in hospitalized

patients2. Anti-hyperglycemic agents in

hospitalized patients3. Preventing hypoglycemia

4. Diabetes care providers in thehospital

5. Self-management in the hospital6. Diabetes self-management edu-

cation in the hospital7. Medical nutrition therapy in the

hospital8. Bedside blood glucose monitor-

ing9. Discharge planning

IX. STRATEGIES FOR IMPROVING DI-ABETES CARE, p. S46

D iabetes is a chronic illness that re-quires continuing medical care andongoing patient self-management

education and support to prevent acutecomplications and to reduce the risk oflong-term complications. Diabetes care iscomplex and requires that many issues,beyond glycemic control, be addressed. Alarge body of evidence exists that sup-ports a range of interventions to improvediabetes outcomes.

These standards of care are intendedto provide clinicians, patients, research-ers, payors, and other interested individ-uals with the components of diabetescare, general treatment goals, and tools toevaluate the quality of care. While indi-vidual preferences, comorbidities, andother patient factors may require modifi-cation of goals, targets that are desirablefor most patients with diabetes are pro-vided. These standards are not intendedto preclude clinical judgment or more ex-tensive evaluation and management of thepatient by other specialists as needed.For more detailed information aboutmanagement of diabetes, refer to refer-ences 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-

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Originally approved 1988. Most recent review/revision October 2010.DOI: 10.2337/dc11-S011© 2011 by the American Diabetes Association. Readers may use this article as long as the work is properly

cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.

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

care.diabetesjournals.org DIABETES CARE, VOLUME 34, SUPPLEMENT 1, JANUARY 2011 S11

tion is listed after each recommendationusing the letters A, B, C, or E.

These standards of care are revisedannually by the ADA’s multidisciplinaryProfessional Practice Committee, incor-porating new evidence. Members of theProfessional Practice Committee and theirdisclosed conflicts of interest are listed onpage S97. Subsequently, as with all Posi-tion Statements, the standards of care arereviewed and approved by the ExecutiveCommittee of ADA’s Board of Directors.

I. CLASSIFICATION ANDDIAGNOSIS OF DIABETES

A. Classification of diabetesThe classification of diabetes includesfour clinical 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 thetreatment of HIV/AIDS or after organtransplantation)

● Gestational diabetes mellitus (GDM)(diabetes diagnosed during pregnancythat is not clearly overt diabetes)

Some patients cannot be clearly classifiedas having type 1 or type 2 diabetes. Clin-ical presentation and disease progressionvary considerably in both types of diabe-tes. Occasionally, patients who otherwisehave type 2 diabetes may present with ke-toacidosis. Similarly, patients with type 1diabetes may have a late onset and slow(but relentless) progression of disease de-spite having features of autoimmune dis-ease. Such difficulties in diagnosis mayoccur in children, adolescents, andadults. The true diagnosis may becomemore obvious over time.

B. Diagnosis of diabetesFor decades, the diagnosis of diabetes wasbased on plasma glucose criteria, eitherthe fasting plasma glucose (FPG) or the

2-h value in the 75-g oral glucose toler-ance test (OGTT) (4).

In 2009, an International ExpertCommittee that included representativesof the ADA, the International DiabetesFederation (IDF), and the European As-sociation for the Study of Diabetes(EASD) recommended the use of the A1Ctest to diagnose diabetes, with a thresholdof �6.5% (5), and ADA adopted this cri-terion in 2010 (4). The diagnostic testshould be performed using a method thatis certified by the National Glycohemo-globin Standardization Program (NGSP)and standardized or traceable to the Dia-betes Control and Complications Trial(DCCT) reference assay. Point-of-careA1C assays are not sufficiently accurate atthis time to use for diagnostic purposes.

Epidemiologic datasets show a simi-lar relationship between A1C and risk ofretinopathy as has been shown for thecorresponding FPG and 2-h plasma glu-cose thresholds. The A1C has several ad-vantages to the FPG and OGTT, includinggreater convenience, since fasting is notrequired; evidence to suggest greater pre-analytical stability; and less day-to-dayperturbations during periods of stress andillness. These advantages must be bal-anced by greater cost, the limited avail-ability of A1C testing in certain regions ofthe developing world, and the incompletecorrelation between A1C and average glu-cose in certain individuals. In addition,A1C levels can vary with patients’ ethnic-ity (6) as well as with certain anemias andhemoglobinopathies. For patients with anabnormal hemoglobin but normal red cellturnover, such as sickle cell trait, an A1Cassay without interference from abnormalhemoglobins should be used (an updatedlist is available at www.ngsp.org/interf.asp). For conditions with abnormal redcell turnover, such as pregnancy, recentblood loss or transfusion, or some ane-mias, the diagnosis of diabetes must em-ploy glucose criteria exclusively.

The established glucose criteria forthe diagnosis of diabetes (FPG and 2-hPG) remain valid as well (Table 2). Just asthere is less than 100% concordance be-tween the FPG and 2-h PG tests, there isnot perfect concordance between A1Cand either glucose-based test. Analyses ofNational Health and Nutrition Examina-tion Survey (NHANES) data indicate that,assuming universal screening of the undi-agnosed, the A1C cut point of �6.5%identifies one-third fewer cases of undiag-nosed diabetes than a fasting glucose cutpoint of �126 mg/dl (7.0 mmol/l) (7).

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 Center 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

• 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

• Evidence from randomized clinical trials with one or more major orthree or more minor methodological flaws that could invalidate theresults

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

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

recommendationE Expert consensus or clinical experience

Standards of Medical Care

S12 DIABETES CARE, VOLUME 34, SUPPLEMENT 1, JANUARY 2011 care.diabetesjournals.org

However, in practice, a large portion ofthe diabetic population remains unawareof their condition. Thus, the lower sensi-tivity of A1C at the designated cut pointmay well be offset by the test’s greaterpracticality, and wider application of amore convenient test (A1C) may actuallyincrease the number of diagnoses made.

As with most diagnostic tests, a testresult diagnostic of diabetes should be re-peated to rule out laboratory error, unlessthe diagnosis is clear on clinical grounds,such as a patient with a hyperglycemiccrisis or classic symptoms of hyperglyce-mia and a random plasma glucose �200mg/dl. It is preferable that the same test berepeated for confirmation, since there willbe a greater likelihood of concurrence inthis case. For example, if the A1C is 7.0%and a repeat result is 6.8%, the diagnosisof diabetes is confirmed. However, if twodifferent tests (such as A1C and FPG) areboth above the diagnostic thresholds, thediagnosis of diabetes is also confirmed.

On the other hand, if two differenttests are available in an individual and theresults are discordant, the test whose re-sult is above the diagnostic cut pointshould be repeated, and the diagnosis ismade on the basis of the confirmed test.That is, if a patient meets the diabetes cri-terion of the A1C (two results �6.5%) butnot the FPG (�126 mg/dl or 7.0 mmol/l),or vice versa, that person should be con-sidered to have diabetes.

Since there is preanalytic and analytic

variability of all the tests, it is also possiblethat when a test whose result was abovethe diagnostic threshold is repeated, thesecond value will be below the diagnosticcut point. This is least likely for A1C,somewhat more likely for FPG, and mostlikely for the 2-h PG. Barring a laboratoryerror, such patients are likely to have testresults near the margins of the thresholdfor a diagnosis. The healthcare profes-sional might opt to follow the patientclosely and repeat the testing in 3– 6months.

The current diagnostic criteria for di-abetes are summarized in Table 2.

C. Categories of increased risk fordiabetes (prediabetes)In 1997 and 2003, The Expert Committeeon Diagnosis and Classification of Diabe-tes Mellitus (8,9) recognized an interme-diate group of individuals whose glucoselevels, although not meeting criteria fordiabetes, are nevertheless too high to beconsidered normal. These persons weredefined as having impaired fasting glu-cose (IFG) (FPG levels 100–125 mg/dl[5.6–6.9 mmol/l]) or impaired glucosetolerance (IGT) (2-h PG values in theOGTT of 140 –199 mg/dl [7.8 –11.0mmol/l]). It should be noted that theWorld Health Organization (WHO) and anumber of other diabetes organizationsdefine the cutoff for IFG at 110 mg/dl (6.1mmol/l).

Individuals with IFG and/or IGT havebeen referred to as having prediabetes, in-dicating the relatively high risk for the fu-ture development of diabetes. IFG andIGT should not be viewed as clinical en-tities in their own right but rather riskfactors for diabetes as well as cardiovas-cular disease (CVD). IFG and IGT are as-sociated with obesi ty (especial lyabdominal or visceral obesity), dyslipide-mia with high triglycerides and/or lowHDL cholesterol, and hypertension.

As is the case with the glucose mea-sures, several prospective studies thatused A1C to predict the progression todiabetes demonstrated a strong, continu-ous association between A1C and subse-quent diabetes. In a systematic review of44,203 individuals from 16 cohort stud-ies with a follow-up interval averaging 5.6years (range 2.8–12 years), those with anA1C between 5.5 and 6.0% had a sub-stantially increased risk of diabetes with5-year incidences ranging from 9–25%.An A1C range of 6.0–6.5% had a 5-yearrisk of developing diabetes between 25–50% and relative risk 20 times higher

compared with an A1C of 5.0% (10). In acommunity-based study of black andwhite adults without diabetes, baselineA1C was a stronger predictor of subse-quent diabetes and cardiovascular eventsthan fasting glucose (11). Other analysessuggest that an A1C of 5.7% is associatedwith diabetes risk similar to that of thehigh-risk participants in the Diabetes Pre-vention Program (DPP).

Hence, it is reasonable to consider anA1C range of 5.7–6.4% as identifying in-dividuals with high risk for future diabe-tes, a state that may be referred to asprediabetes (4). As is the case for individ-uals found to have IFG and IGT, individ-uals with an A1C of 5.7–6.4% should beinformed of their increased risk for diabe-tes as well as CVD and counseled abouteffective strategies to lower their risks (seeIV. PREVENTION/DELAY OF TYPE 2 DIABETES). Aswith glucose measurements, the contin-uum of risk is curvilinear—as A1C rises,the risk of diabetes rises disproportion-ately (10). Accordingly, interventionsshould be most intensive and follow-upparticularly vigilant for those with A1Csabove 6.0%, who should be considered tobe at very high risk.

Table 3 summarizes the categories ofincreased risk for diabetes.

II. TESTING FOR DIABETESIN ASYMPTOMATICPATIENTS

Recommendations● Testing to detect type 2 diabetes and

assess risk for future diabetes in asymp-tomatic people should be considered inadults of any age who are overweight orobese (BMI �25 kg/m2) and who haveone or more additional risk factors fordiabetes (Table 4). In those withoutthese risk factors, testing should beginat age 45 years. (B)

● If tests are normal, repeat testing car-ried out at least at 3-year intervals isreasonable. (E)

Table 2—Criteria for the diagnosis ofdiabetes

A1C �6.5%. The test should be performedin a laboratory using a method that isNGSP certified and standardized to theDCCT assay.*

orFPG �126 mg/dl (7.0 mmol/l). Fasting is

defined as no caloric intake for at least8 h.*

or2-h plasma glucose �200 mg/dl (11.1

mmol/l) during an OGTT. The test shouldbe performed as described by the WorldHealth Organization, using a glucose loadcontaining the equivalent of 75 ganhydrous glucose dissolved in water.*

orIn a patient with classic symptoms of

hyperglycemia or hyperglycemic crisis, arandom plasma glucose �200 mg/dl (11.1mmol/l)

*In the absence of unequivocal hyperglycemia, re-sult should be confirmed by repeat testing.

Table 3—Categories of increased risk for di-abetes (prediabetes)*

FPG 100–125 mg/dl (5.6–6.9 mmol/l): IFGor

2-h plasma glucose in the 75-g OGTT 140–199 mg/dl (7.8–11.0 mmol/l): IGT

orA1C 5.7–6.4%

*For all three tests, risk is continuous, extendingbelow the lower limit of the range and becomingdisproportionately greater at higher ends of therange.

Position Statement


● To test for diabetes or to assess risk offuture diabetes, A1C, FPG, or 2-h 75-gOGTT is appropriate. (B)

● In those identified with increased riskfor future diabetes, identify and, if ap-propriate, treat other CVD 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. Diabetes may be identi-fied anywhere along a spectrum of clinicalscenarios ranging from a seemingly low-risk individual who happens to have glu-cose testing, to a higher-risk individualwhom the provider tests because of highsuspicion of diabetes, to the symptomaticpatient. The discussion herein is primar-ily framed as testing for diabetes in thosewithout symptoms. Testing for diabeteswill also detect individuals at increasedfuture risk for diabetes, herein referred toas having prediabetes.

A. Testing for type 2 diabetes andrisk of future diabetes in adultsType 2 diabetes is frequently not diag-nosed until complications appear, andapproximately one-fourth of all peoplewith diabetes in the U.S. may be undiag-nosed. The effectiveness of early identifi-cation of prediabetes and diabetesthrough mass testing of asymptomatic in-dividuals has not been proven defini-tively, and rigorous trials to provide suchproof are unlikely to occur. However,mathematical modeling studies suggestthat screening independent of risk factorsbeginning at age 30 or 45 years is highlycost-effective (�$11,000 per quality-adjusted life-year gained) (12). Prediabe-tes and diabetes meet established criteriafor conditions in which early detection isappropriate. Both conditions are com-mon and increasing in prevalence and im-pose significant public health burdens.There is a long presymptomatic phase be-fore the diagnosis of type 2 diabetes isusually made. Relatively simple tests areavailable to detect preclinical disease. Ad-ditionally, the duration of glycemic bur-den is a strong predictor of adverseoutcomes, and effective interventions ex-ist to prevent progression of prediabetesto diabetes (see IV. PREVENTION/DELAY OF TYPE

2 DIABETES) and to reduce risk of compli-cations of diabetes (see VI. PREVENTION AND

MANAGEMENT OF DIABETES COMPLICATIONS).Recommendations for testing for dia-

betes in asymptomatic, undiagnosedadults are listed in Table 4. Testing shouldbe considered in adults of any age withBMI �25 kg/m2 and one or more of theknown risk factors for diabetes. Becauseage is a major risk factor for diabetes, test-ing of those without other risk factorsshould begin no later than age 45 years.

Either A1C, FPG, or the 2-h OGTT isappropriate for testing. The 2-h OGTTidentifies people with either IFG or IGTand thus more people at increased risk forthe development of diabetes and CVD. Itshould be noted that the two tests do notnecessarily detect the same individuals.The efficacy of interventions for primaryprevention of type 2 diabetes (13–19)have primarily been demonstrated amongindividuals with IGT, not for individualswith IFG (who do not also have IGT) orfor individuals with specific A1C levels.

The appropriate interval betweentests is not known (20). The rationale forthe 3-year interval is that false negativeswill be repeated before substantial timeelapses, and there is little likelihood thatan individual will develop significant

complications of diabetes within 3 yearsof a negative test result. In the modelingstudy, repeat screening every 3 or 5 yearswas cost-effective (12).

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, or have access to, ap-propriate follow-up testing and care.Conversely, there may be failure to ensureappropriate repeat testing for individualswho test negative. Community screeningmay also be poorly targeted, i.e., it mayfail to reach the groups most at risk andinappropriately test those at low risk (theworried well) or even those already diag-nosed.

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 (21), although the disease remainsrare in the general pediatric population(22). Consistent with recommendationsfor adults, children and youth at in-creased risk for the presence or the devel-opment of type 2 diabetes should betested within the health care setting. Therecommendations of the ADA ConsensusStatement on Type 2 Diabetes in Childrenand Youth (23), with some modifications,are summarized in Table 5.

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. How-ever, evidence from type 1 prevention stud-ies suggests that measurement of isletautoantibodies identifies individuals whoare at risk for developing type 1 diabetes.Such testing may be appropriate in high-risk individuals, such as those with priortransient hyperglycemia or those who haverelatives with type 1 diabetes, in the contextof clinical research studies (see, for ex-ample, http://www2.diabetestrialnet.org).Widespread clinical testing of asymptom-atic low-risk individuals cannot currentlybe recommended, as it would identifyvery few individuals in the general popu-lation who are at risk. Individuals whoscreen positive should be counseledabout their risk of developing diabetes.Clinical studies are being conducted to

Table 4—Criteria for testing for diabetes inasymptomatic adult individuals

1. Testing should be considered in all adultswho are overweight (BMI �25 kg/m2*)and have additional risk factors:

• physical inactivity• first-degree relative with diabetes• high-risk race/ethnicity (e.g., African

American, Latino, Native American,Asian American, Pacific Islander)

• women who delivered a baby weighing�9 lb or were diagnosed with GDM

• hypertension (�140/90 mmHg or ontherapy for hypertension)

• HDL cholesterol level �35 mg/dl (0.90mmol/l) and/or a triglyceride level �250mg/dl (2.82 mmol/l)

• women with polycystic ovariansyndrome (PCOS)

• A1C �5.7%, IGT, or IFG on previoustesting

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

• history of CVD2. In the absence of the above criteria, testing

for diabetes should begin at age 45years.

3. If results are normal, testing should berepeated at least at 3-year intervals, withconsideration of more frequent testingdepending on initial results and riskstatus.

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



test various methods of preventing type 1diabetes, or reversing early type 1 diabe-tes, in those with evidence of autoimmu-nity.

III. DETECTION ANDDIAGNOSIS OFGESTATIONAL DIABETESMELLITUS

Recommendations● Screen for undiagnosed type 2 diabetes

at the first prenatal visit in those withrisk factors, using standard diagnosticcriteria. (B)

● In pregnant women not known to havediabetes, screen for GDM at 24 –28weeks of gestation, using a 75-g 2-hOGTT and the diagnostic cut points inTable 6. (B)

● Screen women with GDM for persistentdiabetes 6–12 weeks postpartum. (E)

● Women with a history of GDM shouldhave lifelong screening for the develop-ment of diabetes or prediabetes at leastevery 3 years. (E)

For many years, GDM was defined as anydegree of glucose intolerance with onsetor first recognition during pregnancy (8),whether or not the condition persisted af-ter pregnancy, and not excluding the pos-sibility that unrecognized glucoseintolerance may have antedated or begunconcomitantly with the pregnancy. Thisdefinition facilitated a uniform strategy

for detection and classification of GDM,but its limitations were recognized formany years. As the ongoing epidemic ofobesity and diabetes has led to more type2 diabetes in women of childbearing age,the number of pregnant women with un-diagnosed type 2 diabetes has increased(24). Because of this, it is reasonable toscreen women with risk factors for type 2diabetes (Table 4) for diabetes at their ini-tial prenatal visit, using standard diagnos-tic criteria (Table 2). Women withdiabetes found at this visit should receivea diagnosis of overt, not gestational, dia-betes.

GDM carries risks for the mother andneonate. The Hyperglycemia and AdversePregnancy Outcomes (HAPO) study (25),a large-scale (�25,000 pregnant women)multinational epidemiologic study, dem-onstrated that risk of adverse maternal,fetal, and neonatal outcomes continu-ously increased as a function of maternalglycemia at 24–28 weeks, even withinranges previously considered normal forpregnancy. For most complications, therewas no threshold for risk. These resultshave led to careful reconsideration of thediagnostic criteria for GDM. After delib-erations in 2008–2009, the InternationalAssociation of Diabetes and PregnancyStudy Groups (IADPSG), an internationalconsensus group with representativesfrom multiple obstetrical and diabetes or-ganizations, including ADA, developedrevised recommendations for diagnosingGDM. The group recommended that allwomen not known to have diabetes un-dergo a 75-g OGTT at 24–28 weeks ofgestation. Additionally, the group devel-oped diagnostic cut points for the fasting,1-h, and 2-h plasma glucose measure-ments that conveyed an odds ratio for ad-verse outcomes of at least 1.75 comparedwith the mean glucose levels in the HAPOstudy. Current screening and diagnosticstrategies, based on the IADPSG state-ment (26), are outlined in Table 6.

These new criteria will significantlyincrease the prevalence of GDM, primar-ily because only one abnormal value, nottwo, is sufficient to make the diagnosis.The ADA recognizes the anticipated sig-nificant increase in the incidence of GDMto be diagnosed by these criteria and issensitive to concerns about the “medical-ization” of pregnancies previously catego-rized as normal. These diagnostic criteriachanges are being made in the context ofworrisome worldwide increases in obe-sity and diabetes rates, with the intent of

optimizing gestational outcomes forwomen and their babies.

Admittedly, there are few data fromrandomized clinical trials regarding ther-apeutic interventions in women who willnow be diagnosed with GDM based ononly one blood glucose value above thespecified cut points (in contrast to theolder criteria that stipulated at least twoabnormal values.) Expected benefits totheir pregnancies and offspring is inferredfrom intervention trials that focused onwomen with more mild hyperglycemiathan identified using older GDM diagnos-tic criteria and that found modest benefits(27,28). The frequency of their follow-upand blood glucose monitoring is not yetclear, but likely to be less intensive thanwomen diagnosed by the older criteria.Additional well-designed clinical studiesare needed to determine the optimal in-tensity of monitoring and treatment ofwomen with GDM diagnosed by the newcriteria (that would not have met the priordefinition of GDM). It is important to notethat 80–90% of women in both of themild GDM studies (whose glucose valuesoverlapped with the thresholds recom-mended herein) could be managed withlifestyle therapy alone.

Because some cases of GDM may rep-resent preexisting undiagnosed type 2 di-abetes, women with a history of GDMshould be screened for diabetes 6 –12weeks postpartum, using nonpregnantOGTT criteria. Women with a history ofGDM have a greatly increased subsequentrisk for diabetes (29) and should be fol-lowed up with subsequent screening forthe development of diabetes or prediabe-tes, as outlined in II. TESTING FOR DIABETES IN

ASYMPTOMATIC PATIENTS.

Table 6—Screening for and diagnosis ofGDM

Perform a 75-g OGTT, with plasma glucosemeasurement fasting and at 1 and 2 h,at 24–28 weeks of gestation in womennot previously diagnosed with overtdiabetes.

The OGTT should be performed in themorning after an overnight fast of atleast 8 h.

The diagnosis of GDM is made when any ofthe following plasma glucose values areexceeded:

• Fasting �92 mg/dl (5.1 mmol/l)• 1 h �180 mg/dl (10.0 mmol/l)• 2 h �153 mg/dl (8.5 mmol/l)

Table 5—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 (Native American, African

American, Latino, Asian American,Pacific Islander)

• Signs of insulin resistance or conditionsassociated with insulin resistance(acanthosis nigricans, hypertension,dyslipidemia, PCOS, or small-for-gestational-age birth weight)

• Maternal history of diabetes or GDMduring the child’s gestation

Age of initiation: age 10 years or at onset ofpuberty, if puberty occurs at a youngerage

Frequency: every 3 years

Position Statement


IV. PREVENTION/DELAYOF TYPE 2 DIABETES

Recommendations● Patients with IGT (A), IFG (E), or an

A1C of 5.7– 6.4% (E) should be re-ferred to an effective ongoing supportprogram targeting weight loss of 7% ofbody weight and increasing physicalactivity to at least 150 min/week ofmoderate activity such as walking.

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

● Based on potential cost savings of diabe-tes prevention, such programs should becovered by third-party payors. (E)

● Metformin therapy for prevention oftype 2 diabetes may be considered inthose at the highest risk for developingdiabetes, such as those with multiplerisk factors, especially if they demon-strate progression of hyperglycemia(e.g., A1C �6%) despite lifestyle inter-ventions. (B)

● Monitoring for the development of di-abetes in those with prediabetes shouldbe 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 (13–19). These interventionsinclude intensive lifestyle modificationprograms that have been shown to be veryeffective (58% reduction after 3 years)and use of the pharmacologic agents met-formin, �-glucosidase inhibitors, orlistat,and thiazolidinediones (TZDs), each ofwhich has been shown to decrease inci-dent diabetes to various degrees. A sum-mary of major diabetes prevention trials isshown in Table 7.

Follow-up of all three large studies oflifestyle intervention has shown sustainedreduction in the rate of conversion to type2 diabetes, with 43% reduction at 20years in the Da Qing study (30), 43% re-duction at 7 years in the Finnish DiabetesPrevention Study (DPS) (31) and 34% re-duction at 10 years in the U.S. DiabetesPrevention Program Outcomes Study(DPPOS) (32). A cost-effectiveness analy-sis suggested that lifestyle interventions asdelivered in the DPP are cost-effective(33). Group delivery of the DPP interven-tion in community settings has the poten-tial to be significantly less expensive whilestill achieving similar weight loss (34).

Based on the results of clinical trialsand the known risks of progression ofprediabetes to diabetes, persons with anA1C of 5.7–6.4%, IGT, or IFG should becounseled on lifestyle changes with goalssimilar to those of the DPP (7% weight

loss and moderate physical activity of atleast 150 min/week). Regarding the moredifficult issue of drug therapy for diabetesprevention, a consensus panel felt thatmetformin should be the only drug con-sidered (39). For other drugs, the issues ofcost, side effects, and lack of persistenceof effect in some studies led the panel tonot recommend their use for diabetes pre-vention. Metformin, which was signifi-cantly less effective than lifestyle in theDPP and DPPOS, reasonably may be rec-ommended for very-high-risk individuals(those with risk factors for diabetes and/orthose with more severe or progressive hy-perglycemia). Of note, in the DPP met-formin was most effective compared tolifestyle in those with BMI of at least 35kg/m2 and was not significantly betterthan placebo in those over age 60 years.

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-

Table 7—Therapies proven effective in diabetes prevention trials

Study (ref.) n Population

Meanage

(years)Duration(years)

Intervention(daily dose)

Incidence incontrolsubjects(%/year)

Relative riskreduction (%)

(95% CI)

3-Yearnumber

needed totreat�

LifestyleFinnish DPS (14) 522 IGT, BMI �25 kg/m2 55 3.2 I-D&E 6 58 (30–70) 8.5DPP (13) 2,161* IGT, BMI �24 kg/m2,

FPG �5.3 mmol/l51 3 I-D&E 10.4 58 (48–66) 6.9

Da Qing (15) 259* IGT (randomized groups) 45 6 G-D&E 14.5 38 (14–56) 7.9Toranomon Study

(35)458 IGT (men), BMI � 24

kg/m2�55 4 I-D&E 2.4 67 (P � 0.043)† 20.6

Indian DPP (19) 269* IGT 46 2.5 I-D&E 23 29 (21–37) 6.4Medications

DPP (13) 2,155* IGT, BMI �24 kg/m2,FPG �5.3 mmol/l

51 2.8 Metformin (1,700mg)

10.4 31 (17–43) 13.9

Indian DPP (19) 269* IGT 46 2.5 Metformin (500 mg) 23 26 (19–35) 6.9STOP-NIDDM (17) 1,419 IGT, FPG �5.6 mmol/l 54 3.2 Acarbose (300 mg) 12.4 25 (10–37) 9.6XENDOS (36) 3,277 BMI �30 kg/m2 43 4 Orlistat (360 mg) 2.4 37 (14–54) 45.5DREAM (18) 5,269 IGT or IFG 55 3.0 Rosiglitazone (8 mg) 9.1 60 (54–65) 6.9Voglibose Ph-3

(37)1,780 IGT 56 3.0 (1-year

Rx)Vogliobose (0.2 mg) 12.0 40 (18–57) 21 (1-year

Rx)

Modified and reprinted with permission (38). Percentage points: �Number needed to treat to prevent 1 case of diabetes, standardized for a 3-year period to improvecomparisons across studies. *Number of participants in the indicated comparisons, not necessarily in entire study. †Calculated from information in the article. DPP, DiabetesPrevention Program; DPS, Diabetes Prevention Study; DREAM, Diabetes Reduction Assessment with Ramipril and Rosiglitazone Medication; STOP-NIDDM, Study toPrevent Non-Insulin Dependent Diabetes; XENDOS, Xenical in the prevention of Diabetes in Obese Subjects. I, individual; G, group; D&E, diet and exercise.



dition should be performed. A focus onthe components of comprehensive care(Table 8) 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 specialinterest 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 beformulated as a collaborative therapeu-tic alliance among the patient and fam-ily, the physician, and other members ofthe health care team. A variety of strat-egies and techniques should be used toprovide adequate education and devel-opment of problem-solving skills in thevarious aspects of diabetes manage-ment. Implementation of the manage-ment plan requires that each aspect isunderstood and agreed to by the patientand the care providers and that the goalsand treatment plan are reasonable. Anyplan should recognize diabetes self-management education (DSME) andongoing diabetes support as an integralcomponent of care. In developing theplan, consideration should be given tothe patient’s age, school or work sched-ule and conditions, physical activity,eating patterns, social situation andcultural factors, and presence of com-plications of diabetes or other medicalconditions.

C. Glycemic control

1. Assessment of glycemic controlTwo primary techniques are available forhealth providers and patients to assess theeffectiveness of the management plan onglycemic control: patient self-monitoringof blood glucose (SMBG) or interstitialglucose, and A1C.

a. Glucose monitoring

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 as a guide tothe success of therapy. (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 (CGM)

in conjunction with intensive insulinregimens can be a useful tool to lowerA1C in selected adults (age �25 years)with type 1 diabetes. (A)

● Although the evidence for A1C-lowering is less strong in children,teens, and younger adults, CGM maybe helpful in these groups. Success cor-relates with adherence to ongoing useof the device. (C)

● CGM may be a supplemental tool toSMBG in those with hypoglycemia un-awareness and/or frequent hypoglyce-mic episodes. (E)

Table 8—Components of the comprehensive diabetes evaluation

Medical history• Age and characteristics of onset of diabetes (e.g., DKA, asymptomatic laboratory finding)• Eating patterns, physical activity habits, nutritional status, and weight history; growth

and development in children 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 activity

patterns, 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 of

foot 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

yearsReferrals

• Annual dilated eye exam• Family planning for women of reproductive age• Registered dietitian for MNT• DSME• Dental examination• Mental health professional, if needed

*See appropriate referrals for these categories.

Position Statement


Major clinical trials of insulin-treated pa-tients that demonstrated the benefits ofintensive glycemic control on diabetescomplications have included SMBG aspart of multifactorial interventions, sug-gesting that SMBG is a component of ef-fective therapy. SMBG allows patients toevaluate their individual response to ther-apy and assess whether glycemic targetsare being achieved. Results of SMBG canbe useful in preventing hypoglycemia andadjusting medications (particularly pran-dial insulin doses), MNT, and physical ac-tivity.

The frequency and timing of SMBGshould be dictated by the particular needsand goals of the patient. 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 these populations,significantly more frequent testing may berequired to reach A1C targets safely with-out hypoglycemia. The optimal frequencyand timing of SMBG for patients with type2 diabetes on noninsulin therapy is un-clear. A meta-analysis of SMBG in non–insulin-treated patients with type 2diabetes concluded that some regimen ofSMBG was associated with a reduction inA1C of 0.4%. However, many of the stud-ies in this analysis also included patienteducation with diet and exercise counsel-ing and, in some cases, pharmacologic in-tervention, making it difficult to assess thecontribution of SMBG alone to improvedcontrol (40). Several recent trials havecalled into question the clinical utility andcost-effectiveness of routine SMBG innon–insulin-treated patients (41–43).

Because the accuracy of SMBG is in-strument and user dependent (44), 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-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 reevaluated pe-riodically.

CGM through the measurement of in-terstitial glucose (which correlates wellwith plasma glucose) is available. Thesesensors require calibration with SMBG,and the latter are still recommended formaking acute treatment decisions. CGMdevices also have alarms for hypo- and

hyperglycemic excursions. Small studiesin selected patients with type 1 diabeteshave suggested that CGM use reduces thetime spent in hypo- and hyperglycemicranges and may modestly improve glyce-mic control. A larger 26-week random-ized trial of 322 type 1 patients showedthat adults age 25 years and older usingintensive insulin therapy and CGM expe-rienced a 0.5% reduction in A1C (from�7.6% to 7.1%) compared to usual in-tensive insulin therapy with SMBG (45).Sensor use in children, teens, and adultsup to age 24 years did not result in signif-icant A1C lowering, and there was no sig-nificant difference in hypoglycemia in anygroup. Importantly, the greatest predictorof A1C-lowering in this study for all age-groups was frequency of sensor use,which was lower in younger age-groups.In a smaller randomized controlled trial of129 adults and children with baselineA1C �7.0%, outcomes combining A1Cand hypoglycemia favored the group uti-lizing CGM, suggesting that CGM is alsobeneficial for individuals with type 1 dia-betes who have already achieved excellentcontrol with A1C �7.0 (46). AlthoughCGM is an evolving technology, emergingdata suggest that, in appropriately se-lected patients who are motivated to wearit most of the time, it may offer benefit.CGM may be particularly useful in thosewith hypoglycemia unawareness and/orfrequent episodes of hypoglycemia, andstudies in this area are ongoing.

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 (44), andhas strong predictive value for diabetescomplications (47,48), 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 have been reached and main-tained. For any individual patient, the fre-

quency 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 (49,50).

The A1C test is subject to certain lim-itations. Conditions that affect erythro-cyte turnover (hemolysis, blood loss) andhemoglobin variants must be considered,particularly when the A1C result does notcorrelate with the patient’s clinical situa-tion (44). In addition, A1C does not pro-vide a measure of glycemic variability orhypoglycemia. For patients prone to gly-cemic variability (especially type 1 pa-tients, or type 2 patients with severeinsulin deficiency), glycemic control isbest judged by the combination of resultsof SMBG testing and the A1C. The A1Cmay also serve as a check on the accuracyof the patient’s meter (or the patient’s re-ported SMBG results) and the adequacy ofthe SMBG testing schedule.

Table 9 contains the correlation be-tween A1C levels and mean plasma glu-cose levels based on data from theinternational A1C-Derived Average Glu-cose (ADAG) trial utilizing frequentSMBG and CGM in 507 adults (83% Cau-casian) with type 1, type 2, and no diabe-

Table 9—Correlation of A1C with averageglucose

A1C (%)

Mean plasma glucose

mg/dl mmol/l

6 126 7.07 154 8.68 183 10.29 212 11.8

10 240 13.411 269 14.912 298 16.5

These estimates are based on ADAG data of �2,700glucose measurements over 3 months per A1C mea-surement in 507 adults with type 1, type 2, and nodiabetes. The correlation between A1C and averageglucose was 0.92 (51). A calculator for convertingA1C results into estimated average glucose (eAG), ineither mg/dl or mmol/l, is available at http://professional.diabetes.org/eAG.



tes (51). The American DiabetesAssociation and American Association ofClinical Chemists have determined thatthe correlation (r � 0.92) is strongenough to justify reporting both an A1Cresult and an estimated average glucose(eAG) result when a clinician orders theA1C test. The table in previous versions ofthe Standards of Medical Care in Diabetesdescribing the correlation between A1Cand mean glucose was derived from rela-tively sparse data (one 7-point profileover 1 day per A1C reading) in the pri-marily Caucasian type 1 diabetic partici-pants in the DCCT (52). Cliniciansshould note that the numbers in the tableare now different, as they are based on�2,800 readings per A1C in the ADAGtrial.

In the ADAG trial, there were no sig-nificant differences among racial and eth-nic groups in the regression lines betweenA1C and mean glucose, although therewas a trend toward a difference betweenAfrican/African American participantsand Caucasian ones that might have beensignificant had more African/AfricanAmerican participants been studied. A re-cent study comparing A1C with CGMdata in 48 type 1 diabetic children founda highly statistically significant correla-tion between A1C and mean blood glu-cose, although the correlation (r � 0.7)was significantly lower than in the ADAGtrial (53). Whether there are significantdifferences in how A1C relates to averageglucose in children or in African Ameri-can patients is an area for further study.For the time being, the question has notled to different recommendations abouttesting A1C or to different interpretationsof the clinical meaning of given levels ofA1C in those populations.

For patients in whom A1C/eAG andmeasured blood glucose appear discrep-ant, clinicians should consider the possi-bilities of hemoglobinopathy or alteredred cell turnover, and the options of morefrequent and/or different timing of SMBGor use of CGM. Other measures of chronicglycemia such as fructosamine are avail-able, but their linkage to average glucoseand their prognostic significance are notas clear as is the case for A1C.

2. Glycemic goals in adults

Recommendations● Lowering A1C to below or around 7%

has been shown to reduce microvascu-lar and neuropathic complications ofdiabetes and, if implemented soon after

the diagnosis of diabetes, is associatedwith long-term reduction in macrovas-cular disease. Therefore, a reasonableA1C goal for many nonpregnant adultsis �7%. (B)

● Because additional analyses from sev-eral randomized trials suggest a smallbut incremental benefit in microvascu-lar outcomes with A1C values closer tonormal, providers might reasonablysuggest more stringent A1C goals forselected individual patients, if this canbe achieved without significant hypo-glycemia or other adverse effects oftreatment. Such patients might includethose with short duration of diabetes,long life expectancy, and no significantCVD. (B)

● Conversely, less stringent A1C goalsmay be appropriate for patients with ahistory of severe hypoglycemia, limitedlife expectancy, advanced microvascu-lar or macrovascular complications, ex-tensive comorbid conditions, and thosewith longstanding diabetes in whomthe general goal is difficult to attain de-spite DSME, appropriate glucose mon-itoring, and effective doses of multipleglucose-lowering agents including in-sulin. (C)

Glycemic control is fundamental to themanagement of diabetes. The DCCT (47)(in patients with type 1 diabetes), the Ku-mamoto study (54), and the UK Prospec-tive Diabetes Study (UKPDS) (55,56)(both in patients with type 2 diabetes)were prospective, randomized, controlledtrials of intensive versus standard glyce-mic control in patients with relatively re-cently diagnosed diabetes. These trialsshowed definitively that improved glyce-mic control is associated with signifi-cantly decreased rates of microvascular(retinopathy and nephropathy) and neu-ropathic complications. Follow up of theDCCT cohorts in the Epidemiology of Di-abetes Interventions and Complications(EDIC) study (57,58) and of the UKPDScohort (59) has shown persistence ofthese microvascular benefits in previouslyintensively treated subjects, even thoughtheir glycemic control has been equiva-lent to that of previous standard arm sub-jects during follow-up.

Subsequent trials in patients withmore long-standing type 2 diabetes, de-signed primarily to look at the role ofintensive glycemic control on cardiovas-cular outcomes also confirmed a benefit,although more modest, on onset or pro-gression of microvascular complications.

The Veterans Affairs Diabetes Trial(VADT) showed significant reductions inalbuminuria with intensive (achieved me-dian A1C 6.9%) compared to standardglycemic control, but no difference in ret-inopathy and neuropathy (60,61). TheAction in Diabetes and Vascular Disease:Preterax and Diamicron Modified ReleaseControlled Evaluation (ADVANCE) studyof intensive versus standard glycemiccontrol in type 2 diabetes found a statis-tically significant reduction in albumin-uria with an A1C target of �6.5%(achieved median A1C 6.3%) comparedto standard therapy achieving a medianA1C of 7.0% (62). Recent analyses fromthe Action to Control Cardiovascular Riskin Diabetes (ACCORD) trial have shownlower rates of measures of microvascularcomplications in the intensive glycemiccontrol arm compared with the standardarm (63,64).

Epidemiological analyses of theDCCT and UKPDS (47,48) 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 microvas-cular complications, albeit the absoluterisk reductions become much smaller.Given the substantially increased risk ofhypoglycemia (particularly in those withtype 1 diabetes, but also in the recent type2 trials), the concerning mortality find-ings in the ACCORD trial (65), and therelatively much greater effort required toachieve near-normoglycemia, the risks oflower targets may outweigh the potentialbenefits on microvascular complicationson a population level. However, selectedindividual patients, especially those withlittle comorbidity and long life expect-ancy (who may reap the benefits of fur-ther lowering of glycemia below 7%) may,at patient and provider judgment, adoptglycemic targets as close to normal as pos-sible as long as significant hypoglycemiadoes not become a barrier.

Whereas many epidemiologic studiesand meta-analyses (66,67) have clearlyshown a direct relationship between A1Cand CVD, the potential of intensive glyce-mic control to reduce CVD has been lessclearly defined. In the DCCT, there was atrend toward lower risk of CVD eventswith intensive control. However, 9-yearpost-DCCT follow-up of the cohort has

Position Statement


shown that participants previously ran-domized to the intensive arm had a 42%reduction (P � 0.02) in CVD outcomesand a 57% reduction (P � 0.02) in therisk of nonfatal myocardial infarction(MI), stroke, or CVD death comparedwith those previously in the standard arm(68). The benefit of intensive glycemiccontrol in this type 1 cohort has recentlybeen shown to persist for several decades(69).

The UKPDS trial of type 2 diabetesobserved a 16% reduction in cardiovascu-lar complications (combined fatal or non-fatal MI and sudden death) in theintensive glycemic control arm, althoughthis difference was not statistically signif-icant (P � 0.052), and there was no sug-gestion of benefit on other CVD outcomessuch as stroke. However, 10 years of fol-low-up of the UKPDS cohort demon-strated, for participants originallyrandomized to intensive glycemic controlcompared with those randomized to con-ventional glycemic control, long-term re-ductions in MI (15% with sulfonylurea orinsulin as initial pharmacotherapy, 33%with metformin as initial pharmacother-apy, both statistically significant) and inall-cause mortality (13 and 27%, respec-tively, both statistically significant) (59).

Re su l t s o f th r ee l a rge t r i a l s(ACCORD, ADVANCE, and VADT) sug-gested no significant reduction in CVDoutcomes with intensive glycemic controlin these populations, who had more ad-vanced diabetes than UKPDS partici-pants. Details of these three studies arereviewed extensively in a recent ADA po-sition statement (70).

The glycemic contro l arm ofACCORD was halted early due to thefinding of an increased rate of mortality inthe intensive arm compared with the stan-dard arm (1.41% vs. 1.14% per year; HR1.22 [95% CI 1.01 to 1.46]); with a sim-ilar increase in cardiovascular deaths. Theprimary outcome of ACCORD (MI,stroke, or cardiovascular death) waslower in the intensive glycemic controlgroup, due to a reduction in nonfatal MI,but this reduction was not statistically sig-nificant when the study was terminated(65).

The potential cause of excess deathsin the intensive group of the ACCORDhas been difficult to pinpoint. Explor-atory analyses of the mortality findings ofACCORD (evaluating variables includingweight gain, use of any specific drug ordrug combination, and hypoglycemia)were reportedly unable to identify a clear

explanation for the excess mortality in theintensive arm. The ACCORD investiga-tors subsequently published additionalanalyses showing no increase in mortalityin the intensive arm participants whoachieved A1C levels �7% or in those wholowered their A1C quickly after trial en-rollment. In fact, the converse was ob-served—those at highest risk for mortalitywere participants in the intensive armwith the highest A1C levels (71).

The primary outcome of ADVANCEwas a combination of microvascularevents (nephropathy and retinopathy)and major adverse cardiovascular events(MI, stroke, and cardiovascular death).Intensive glycemic control significantlyreduced the primary end point, althoughthis was due to a significant reduction inthe microvascular outcome, primarily de-velopment of macroalbuminuria, with nosignificant reduction in the macrovascu-lar outcome. There was no difference inoverall or cardiovascular mortality be-tween the intensive compared with thestandard glycemic control arms (62).

The VADT randomized participantswith type 2 diabetes uncontrolled on in-sulin or maximal dose oral agents (me-dian entry A1C 9.4%) to a strategy ofintensive glycemic control (goal A1C�6.0%) or standard glycemic control,with a planned A1C separation of at least1.5%. The primary outcome of the VADTwas a composite of CVD events. The cu-mulative primary outcome was nonsig-nificantly lower in the intensive arm (60).

Unlike the UKPDS, which was carriedout in patients with newly diagnosed di-abetes, all three of the recent type 2 car-diovascular trials were conducted inparticipants with established diabetes(mean duration 8–11 years) and eitherknown CVD or multiple risk factors, sug-gesting the presence of established ath-erosclerosis. Subset analyses of the threetrials suggested a significant benefit of in-tensive glycemic control on CVD in par-ticipants with shorter duration ofdiabetes, lower A1C at entry, and/or orabsence of known CVD. The DCCT-EDICstudy and the long-term follow-up of theUKPDS cohort both suggest that intensiveglycemic control initiated soon after diag-nosis of diabetes in patients with a lowerlevel of CVD risk may impart long-termprotection from CVD events. As is thecase with microvascular complications, itmay be that glycemic control plays agreater role before macrovascular diseaseis well developed and minimal or no rolewhen it is advanced. Consistent with this

concept, data from an ancillary study ofthe VADT demonstrated that intensiveglycemic control was quite effective in re-ducing CVD events in individuals withless atherosclerosis at baseline (assessedby coronary calcium) but not in personswith more extensive baseline atheroscle-rosis (72).

The evidence for a cardiovascularbenefit of intensive glycemic control pri-marily rests on long-term follow-up ofstudy cohorts treated early in the courseof type 1 and type 2 diabetes and subsetanalyses of ACCORD, ADVANCE, andVADT. A recent group-level meta-analysis of the latter three trials suggeststhat glucose lowering has a modest (9%)but statistically significant reduction inmajor CVD outcomes, primarily nonfatalMI, with no significant effect on mortality.A prespecified subgroup analysis sug-gested that major CVD outcome reduc-tion occurred in patients without knownCVD at baseline (HR 0.84 [95% CI 0.74–0.94]) (73). Conversely, the mortalityfindings in ACCORD and subgroup anal-yses of VADT suggest that the potentialrisks of very intensive glycemic controlmay outweigh its benefits in some pa-tients, such as those with very long dura-tion of diabetes, known history of severehypoglycemia, advanced atherosclerosis,and advanced age/frailty. Certainly, pro-viders should be vigilant in preventing se-vere hypoglycemia in patients withadvanced disease and should not aggres-sively attempt to achieve near-normalA1C levels in patients in whom such atarget cannot be reasonably easily andsafely achieved.

Recommended glycemic goals formany nonpregnant adults are shown inTable 10. The recommendations arebased on those for A1C values, with listedblood glucose levels that appear to corre-late with achievement of an A1C of �7%.Less-stringent treatment goals may be ap-propriate for adults with limited life ex-pectancies or advanced vascular disease.Glycemic goals for children are providedin VII.A.1.a. Glycemic control. Severe orfrequent hypoglycemia is an absolute in-dication for the modification of treatmentregimens, including setting higher glyce-mic goals.

The issue of pre- versus postprandialSMBG targets is complex (74). 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 (75). 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 landmark glycemic control tri-als such as the DCCT and UKPDS reliedoverwhelmingly on preprandial SMBG.Additionally, a randomized controlledtrial in patients with known CVD foundno CVD benefit of insulin regimens tar-geting postprandial glucose comparedwith targeting preprandial glucose (76). Areasonable recommendation for post-prandial testing and targets is that for in-dividuals who have premeal glucosevalues within target but have A1C valuesabove target, monitoring postprandialplasma glucose (PPG) 1–2 h after the startof the meal and treatment aimed at reduc-ing PPG values to �180 mg/dl may helplower A1C.

As regards goals for glycemic controlfor women with GDM, recommendationsfrom the Fifth International Workshop-Conference on Gestational Diabetes (77)were to target maternal capillary glucoseconcentrations of:

• 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 (6.7mmol/l)

For women with preexisting type 1 ortype 2 diabetes who become pregnant, arecent consensus statement (78) recom-mended the following as optimal glyce-mic goals, if they can be achieved withoutexcessive hypoglycemia:

● premeal, bedtime, and overnight glu-cose 60–99 mg/dl (3.3–5.4 mmol/l)

● peak postprandial glucose 100 –129mg/dl (5.4–7.1mmol/l)

● A1C �6.0%

D. Pharmacologic and overallapproaches to treatment

1. Therapy for type 1 diabetesThe DCCT clearly showed that intensiveinsulin therapy (three or more injectionsper day of insulin, or continuous subcu-taneous insulin infusion (CSII) (insulinpump therapy) was a key part of im-proved glycemia and better outcomes(47,68). At the time of the study, therapywas carried out with short- and interme-diate-acting human insulins. Despite bet-ter microvascular outcomes, intensiveinsulin therapy was associated with a highrate in severe hypoglycemia (62 episodesper 100 patient-years of therapy). Sincethe time of the DCCT, a number of rapid-acting and long-acting insulin analogshave been developed. These analogs areassociated with less hypoglycemia withequal A1C-lowering in type 1 diabetes(79,80).

Therefore, recommended therapy for

type 1 diabetes consists of the followingcomponents: 1) use of multiple dose in-sulin injections (three to four injectionsper day of basal and prandial insulin) orCSII therapy; 2) matching of prandial in-sulin to carbohydrate intake, premealblood glucose, and anticipated activity;and 3) for many patients (especially if hy-poglycemia is a problem), use of insulinanalogs. There are excellent reviews avail-able that guide the initiation and manage-ment of insulin therapy to achieve desiredglycemic goals (3,79,81).

Because of the increased frequency ofother autoimmune diseases in type 1 dia-betes, screening for thyroid dysfunction,vitamin B12 deficiency, or celiac diseaseshould be considered based on signs andsymptoms. Periodic screening in absenceof symptoms has been recommended, butthe effectiveness and optimal frequencyare unclear.

2. Therapy for type 2 diabetesThe ADA and the EASD published an ex-pert consensus statement on the approachto management of hyperglycemia in indi-viduals with type 2 diabetes (82). High-lights of this approach are: intervention atthe time of diagnosis with metformin incombination with lifestyle changes (MNTand exercise) and continuing timely aug-mentation of therapy with additionalagents (including early initiation of insu-lin therapy) as a means of achieving andmaintaining recommended levels of gly-cemic control (i.e., A1C �7% for mostpatients). As A1C targets are not achieved,treatment intensification is based on theaddition of another agent from a differentclass. The overall objective is to achieveand maintain glycemic control and tochange interventions when therapeuticgoals are not being met.

The algorithm took into account theevidence for A1C-lowering of the individ-ual interventions, their additive effects,and their expense. The precise drugs usedand their exact sequence may not be asimportant as achieving and maintainingglycemic targets safely. Medications notincluded in the consensus algorithm, ow-ing to less glucose-lowering effectiveness,limited clinical data, and/or relative ex-pense, still may be appropriate choices inindividual patients to achieve glycemicgoals. Initiation of insulin at time of diagno-sis is recommended for individuals present-ing with weight loss or other severehyperglycemic symptoms or signs.

Table 10—Summary of glycemic recommendations for many nonpregnant adults withdiabetes

A1C �7.0%*Preprandial capillary plasma glucose 70–130 mg/dl* (3.9–7.2 mmol/l)Peak postprandial capillary plasma glucose† �180 mg/dl* (�10.0 mmol/l)

• Goals should be individualized based on*:• duration of diabetes• age/life expectancy• comorbid conditions• known CVD or advanced microvascular

complications• hypoglycemia unawareness• individual patient considerations

• More or less stringent glycemic goals maybe appropriate for individual patients.

• Postprandial glucose may be targeted ifA1C goals are not met despite reachingpreprandial glucose goals.

Postprandial glucose measurements should be made 1–2 h after the beginning of the meal, generally peaklevels in patients with diabetes.

Position Statement


E. Diabetes self-managementeducation

Recommendations● People with diabetes should receive di-

abetes self-management education(DSME) according to national stan-dards when their diabetes is diagnosedand as needed thereafter. (B)

● Effective self-management and qualityof life are the key outcomes of DSMEand should be measured and moni-tored as part of care. (C)

● DSME should address psychosocial is-sues, since emotional well-being is as-sociated with posit ive diabetesoutcomes. (C)

● Because DSME can result in cost-savings and improved outcomes (B),DSME should be adequately reim-bursed by third-party payors. (E)

DSME is an essential element of diabetescare (83–88), and national standards forDSME (89) are based on evidence for itsbenefits. Education helps people with di-abetes initiate effective self-managementand cope with diabetes when they are firstdiagnosed. Ongoing DSME and supportalso help people with diabetes maintaineffective self-management throughout alifetime of diabetes as they face new chal-lenges and treatment advances becomeavailable. DSME helps patients optimizemetabolic control, prevent and managecomplications, and maximize quality oflife in a cost-effective manner (90).

DSME is the ongoing process of facil-itating the knowledge, skill, and abilitynecessary for diabetes self-care. This pro-cess incorporates the needs, goals, and lifeexperiences of the person with diabetes.The overall objectives of DSME are to sup-port informed decision-making, self-carebehaviors, problem-solving, and activecollaboration with the health care team toimprove clinical outcomes, health status,and quality of life in a cost-effective man-ner (89).

Current best practice of DSME is askills-based approach that focuses onhelping those with diabetes to make in-formed self-management choices. DSMEhas changed from a didactic approach fo-cusing on providing information to moretheoretically based empowerment modelsthat focus on helping those with diabetesmake informed self-management deci-sions. Care of diabetes has shifted to anapproach that is more patient centeredand places the person with diabetes andhis or her family at the center of the care

model working in collaboration withhealth care professionals. Patient-centered care is respectful of and respon-sive to individual patient preferences,needs, and values and ensures that patientvalues guide all decision making (91).

Evidence for the benefits of DSMEMultiple studies have found that DSME isassociated with improved diabetesknowledge and improved self-care behav-ior (83), improved clinical outcomes suchas lower A1C (84,85,87,88,92), lowerself-reported weight (83), improved qual-ity of life (86,93), healthy coping (94),and lower costs (95). Better outcomeswere reported for DSME interventionsthat were longer and included follow-upsupport (83,96–99), that were culturally(100,101) and age appropriate (102,103)and tailored to individual needs and pref-erences, and that addressed psychosocialissues and incorporated behavioral strat-egies (83,87,104–106). Both individualand group approaches have been foundeffective (107–110). There is growing ev-idence for the role of community healthworkers and peer (111,112) and lay lead-ers (113) in delivering DSME and supportin addition to the core team (114).

Diabetes education is associated withincreased use of primary and preventiveservices and lower use of acute, inpatienthospital services (95). Patients who par-ticipate in diabetes education are morelikely to follow best practice treatmentrecommendations, particularly amongthe Medicare population, and have lowerMedicare and commercial claim costs(115).

National standards for DSMENational standards for DSME are de-signed to define quality DSME and to as-sist diabetes educators in a variety ofsettings to provide evidence-based educa-tion (89). The standards, most recentlyrevised in 2007, are reviewed and up-dated every 5 years by a task force repre-senting key organizations involved in thefield of diabetes education and care.

Reimbursement for DSMEDSME, when provided by a program thatmeets the national standards for DSME andis recognized by the ADA or other approvalbodies, is reimbursed as partof the Medicareprogram as overseen by the Centers for Medi-care and Medicaid Services (CMS) (www.cms.hhs.gov/DiabetesSelfManagement).DSME is also covered by a growing numberof other health insurance plans.

F. Medical nutrition therapy

General recommendations● Individuals who have prediabetes or di-

abetes should receive individualizedmedical nutrition therapy (MNT) asneeded to achieve treatment goals, pref-erably provided by a registered dietitianfamiliar with the components of diabe-tes MNT. (A)

● Because MNT can result in cost-savingsand improved outcomes (B), MNTshould be adequately covered by insur-ance and 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-carbohydrate,low-fat calorie-restricted, or Mediterra-nean diets may be effective in the short-term (up to 2 years). (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)

Recommendations for primaryprevention of diabetes● Among individuals at high risk for de-

veloping type 2 diabetes, structuredprograms that emphasize lifestylechanges that include moderate weightloss (7% body weight) and regularphysical activity (150 min/week),with dietary strategies including re-duced calories and reduced intake ofdietary fat, can reduce the risk for de-veloping diabetes and are thereforerecommended. (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)



Recommendations for managementof diabetes

Macronutrients in diabetesmanagement● The best mix of carbohydrate, protein,

and fat may be adjusted to meet themetabolic goals and individual prefer-ences of the person with diabetes. (E)

● Monitoring carbohydrate, whether bycarbohydrate counting, choices, or ex-perience-based estimation, remains akey strategy in achieving glycemic con-trol. (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)

● Saturated fat intake should be �7% oftotal calories. (A)

● Reducing intake of trans fat lowers LDLcholesterol and increases HDL choles-terol (A), therefore intake of trans fatshould be minimized. (E)

Other nutrition recommendations● If adults with diabetes choose to use

alcohol, 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)

● Individualized meal planning shouldinclude optimization of food choices tomeet recommended dietary allowance(RDA)/dietary reference intake (DRI)for all micronutrients. (E)

MNT is an integral component of diabetesprevention, management, and self-management education. In addition to itsrole in preventing and controlling diabe-tes, ADA recognizes the importance ofnutrition as 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 (116). Achieving nutri-tion-related goals requires a coordinatedteam effort that includes the active in-

volvement of the person with prediabetesor diabetes. Because of the complexity ofnutrition issues, it is recommended that aregistered dietitian who is knowledgeableand skilled in implementing nutritiontherapy into diabetes management andeducation be the team member who pro-vides MNT.

Clinical trials/outcome studies ofMNT have reported decreases in A1C at3–6 months ranging from 0.25% to 2.9%with higher reductions seen in type 2 di-abetes of shorter duration. Multiple stud-ies have demonstrated susta inedimprovements in A1C at 12 months andlonger when an Registered Dietitian pro-vided follow-up visits ranging frommonthly to three sessions per year (117–124). Studies in nondiabetic people sug-gest that MNT reduces LDL cholesterol by15–25 mg/dl up to 16% (125) and sup-port a role for lifestyle modification intreating hypertension (125,126).

Because of the effects of obesity oninsulin resistance, weight loss is an im-portant therapeutic objective for over-weight or obese individuals withprediabetes or diabetes (127). 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 (128); long-er-term studies (52 weeks) showed mixedeffects on A1C in adults with type 2 dia-betes (129–131), and in some studies re-sults were confounded by pharmacologicweight loss therapy. A systematic reviewof 80 weight loss studies of �1 year induration demonstrated that moderateweight loss achieved through diet alone,diet and exercise, and meal replacementscan be achieved and maintained (4.8–8%weight loss at 12 months) (132). The mul-tifactorial intensive lifestyle interventionemployed in the DPP, which included re-duced intake of fat and calories, led toweight loss averaging 7% at 6 months andmaintenance of 5% weight loss at 3 years,associated with a 58% reduction in inci-dence of type 2 diabetes (13). A recentrandomized controlled trial looking athigh-risk individuals in Spain showed theMediterranean dietary pattern reducedthe incidence of diabetes in the absence ofweight loss by 52% compared to the low-fat control group (133). Look AHEAD(Action for Health in Diabetes) is a largeclinical trial designed to determinewhether long-term weight loss will im-prove glycemia and prevent cardiovascu-

lar events in subjects with type 2 diabetes.One-year results of the intensive lifestyleintervention in this trial show an average8.6% weight loss, significant reduction ofA1C, and reduction in several CVD riskfactors (134), with benefits sustained at 4years (135). When completed, the LookAHEAD study should provide insight intothe effects of long-term weight loss on im-portant 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 (136,137); however, at 1year, the difference in weight loss be-tween the low-carbohydrate and low-fatdiets was not significant, and weight losswas modest with both diets. A study com-paring low-fat to low-carbohydrate diets,both combined with a comprehensivelifestyle program, showed the sameamount of weight loss (7%) at 2 years inboth groups (138). 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 (139). 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 (137). 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(140). In a 2-year dietary interventionstudy, Mediterranean and low-carbohy-drate diets were found to be effective andsafe alternatives to a low-fat diet forweight reduction in moderately obeseparticipants (141).

The RDA for digestible carbohydrateis 130 g/day and is based on providingadequate glucose as the required fuel forthe central nervous system without reli-ance on glucose production from ingestedprotein or fat. Although brain fuel needscan be met on lower-carbohydrate diets,long term metabolic effects of very-low-carbohydrate diets are unclear, and suchdiets eliminate many foods that are im-

Position Statement


portant sources of energy, fiber, vitamins,and minerals and are important in dietarypalatability (142).

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. It must be clearlyrecognized that regardless of the macronu-trient mix, total caloric intake must be ap-propriate to weight management goal.Further, individualization of the macronu-trient composition will depend on the met-abolic status of the patient (e.g., lipidprofile, renal function) and/or food prefer-ences. Plant-based diets (vegan or vegetar-ian) that are well planned and nutritionallyadequate have also been shown to improvemetabolic control (143,144).

The primary goal with respect to di-etary fat in individuals with diabetes is tolimit saturated fatty acids, trans fatty acids,and cholesterol intake so as to reduce riskfor CVD. Saturated and trans fatty acids arethe principal dietary determinants ofplasma LDL cholesterol. There is a lack ofevidence on the effects of specific fatty acidson people with diabetes, so the recom-mended goals are consistent with those forindividuals with CVD (125,145).

Reimbursement for MNTMNT, when delivered by a registered dietitianaccording to nutrition practice guidelines, isreimbursedaspartof theMedicareprogramasoverseen by the Centers for Medicare andMedicaidServices(CMS)(www.cms.hhs.gov/medicalnutritiontherapy).

G. 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)

Exercise is an important part of the diabe-tes management plan. Regular exercisehas been 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 in

high-risk individuals (13–15). Structuredexercise interventions of at least 8 weeks’duration have been shown to lower A1Cby an average of 0.66% in people withtype 2 diabetes, even with no significantchange in BMI (146). Higher levels of ex-ercise intensity are associated with greaterimprovements in A1C and in fitness(147). A new joint position statement ofthe American Diabetes Association andthe American College of Sports Medicinesummarizes the evidence for the benefitsof exercise in people with type 2 diabetes(148).

Frequency and type of exerciseThe U.S. Department of Health and Hu-man Services’ Physical Activity Guide-lines for Americans (149) suggest thatadults over age 18 years do 150 min/weekof moderate-intensity, or 75 min/week ofvigorous aerobic physical activity, or anequivalent combination of the two. In ad-dition, the guidelines suggest that adultsalso do muscle-strengthening activitiesthat involve all major muscle groups twoor more days per week. The guidelinessuggest that adults over age 65 years, orthose with disabilities, follow the adultguidelines if possible or (if this is not pos-sible) be as physically active as they areable. Studies included in the meta-analysis of effects of exercise interventionson glycemic control (146) had a meannumber of sessions per week of 3.4, witha mean of 49 min/session. The DPP life-style intervention, which included 150min/week of moderate intensity exercise,had a beneficial effect on glycemia inthose with prediabetes. Therefore, itseems reasonable to recommend that peo-ple with diabetes try to follow the physicalactivity guidelines for the general popula-tion.

Progressive resistance exercise im-proves insulin sensitivity in older menwith type 2 diabetes to the same or even agreater extent as aerobic exercise (150).Clinical trials have provided strong evi-dence for the A1C-lowering value of re-sistance training in older adults with type2 diabetes (151,152) and for an additivebenefit of combined aerobic and resis-tance exercise in adults with type 2 diabe-tes (153).

Evaluation of the diabetic patientbefore recommending an exerciseprogramPrior guidelines suggested that before rec-ommending a program of physical activ-ity, the provider should assess patients

with multiple cardiovascular risk factorsfor coronary artery disease (CAD). As dis-cussed more fully in VI.A.5. Coronaryheart disease screening and treatment, thearea of screening asymptomatic diabeticpatients for CAD remains unclear, and arecent ADA consensus statement on thisissue concluded that routine screening isnot recommended (154). Providersshould use clinical judgment in this area.Certainly, 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 footlesions, and unstable proliferative reti-nopathy. The patient’s age and previousphysical activity level should be consid-ered.

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 (155);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). Hy-poglycemia is rare in diabetic individualswho are not treated with insulin or insulinsecretagogues, and no preventive mea-sures for hypoglycemia are usually ad-vised in these cases.

Exercise in the presence of specificlong-term complications of diabetesRetinopathy. In the presence of prolifer-ative diabetic retinopathy (PDR) or severenonproliferative diabetic retinopathy(NPDR), vigorous aerobic or resistanceexercise may be contraindicated becauseof the risk of triggering vitreous hemor-rhage or retinal detachment (156).Peripheral neuropathy. Decreased painsensation in the extremities results in in-



creased risk of skin breakdown and infec-tion and of Charcot joint destruction.Prior recommendations have advisednon–weight-bearing exercise for patientswith severe peripheral neuropathy. How-ever, studies have shown that moderate-intensity walking may not lead toincreased risk of foot ulcers or re-ulceration in those with peripheral neu-ropathy (157). All individuals withperipheral neuropathy should wearproper footwear and examine their feetdaily to detect lesions early. Anyone witha foot injury or open sore should be re-stricted to non–weight-bearing activities.Autonomic neuropathy. Autonomic neu-ropathy can increase the risk of exercise-induced injury or adverse event throughdecreased cardiac responsiveness to exer-cise, postural hypotension, impairedthermoregulation, impaired night visiondue to impaired papillary reaction, andunpredictable carbohydrate delivery fromgastroparesis predisposing to hypoglyce-mia (158). Autonomic neuropathy is alsostrongly associated with CVD in peoplewith diabetes (159,160). People with di-abetic autonomic neuropathy should un-dergo cardiac investigation beforebeginning physical activity more intensethan that to which they are accustomed.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, and there is likely no need for anyspecific exercise restrictions for peoplewith diabetic kidney disease (161).

H. 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 and diabetes-related dis-tress, anxiety, eating disorders, andcognitive impairment when self-management is poor. (C)

Psychological and social problems canimpair the individual’s (162–165) or fam-ily’s ability to carry out diabetes care tasksand therefore compromise health status.There are opportunities for the clinicianto assess psychosocial status in a timelyand efficient manner so that referral forappropriate services can be accom-plished.

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. Patients are likelyto exhibit psychological vulnerability atdiagnosis and when their medical statuschanges, e.g., the end of the honeymoonperiod, when the need for intensifiedtreatment is evident, and when complica-tions are discovered (164).

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, diabetes-related distress (166), re-sources (financial, social, and emotional)(167), and psychiatric history (168 –170). Screening tools are available for anumber of these areas (105). Indicationsfor referral to a mental health specialistfamiliar with diabetes management mayinclude: gross noncompliance with med-ical regimen (by self or others) (170), de-pression with the possibility of self-harm,debilitating anxiety (alone or with depres-sion), indications of an eating disorder(171), or cognitive functioning thatsignificantly impairs judgment. It ispreferable to incorporate psychologicalassessment and treatment into routinecare rather than waiting for identificationof a specific problem or deterioration inpsychological status (105). Although theclinician may not feel qualified to treatpsychological problems, utilizing the pa-tient-provider relationship as a founda-tion for further treatment can increase thelikelihood that the patient will accept re-ferral for other services. It is important toestablish that emotional well-being is partof diabetes management.

I. When treatment goals are not metFor a variety of reasons, some people withdiabetes and their health care providersdo not achieve the desired goals of treat-ment (Table 10). Re-thinking the treat-ment regimen may require assessment of

barriers including income, health literacy,diabetes distress, depression, and com-peting demands, including those relatedto family responsibilities and dynamics.Other strategies may include culturallyappropriate and enhanced DSME, co-management with a diabetes team, refer-ral to a medical social worker forassistance with insurance coverage, orchange in pharmacological therapy. Initi-ation of or increase in SMBG, utilizationof CGM, frequent contact with the pa-tient, or referral to a mental health profes-sional or physician with special expertisein diabetes may be useful. Providing pa-tients with an algorithm for self-titrationof insulin doses based on SMBG resultsmay be helpful for type 2 patients whotake insulin (172).

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 aftertreatment 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, to partially reverse hypo-glycemia unawareness and reduce riskof future episodes. (B)

Hypoglycemia is the leading limiting fac-tor in the glycemic management of type 1and insulin-treated type 2 diabetes (173).Mild hypoglycemia may be inconvenientor frightening to patients with diabetes,and more severe hypoglycemia can causeacute harm to the person with diabetes orothers, if it causes falls, motor vehicle ac-cidents, or other injury. A large cohortstudy suggested that among older adultswith type 2 diabetes, a history of severehypoglycemia was associated with greater

Position Statement


risk of dementia (174). Conversely, evi-dence from the DCCT/EDIC trial, whichinvolved younger type 1 patients, sug-gested no association of frequency of se-vere hypoglycemia with cognitive decline(175). Treatment of hypoglycemia(plasma glucose �70 mg/dl) requires in-gestion of glucose- or carbohydrate-containing foods. The acute glycemicresponse correlates better with the glu-cose content than with the carbohydratecontent of the food. Although pure glu-cose is the preferred treatment, any formof carbohydrate that contains glucose willraise blood glucose. Added fat may retardand then prolong the acute glycemic re-sponse. Ongoing activity of insulin or in-sul in secretagogues may lead torecurrence of hypoglycemia unless fur-ther food is ingested 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 counterregulatory 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 counterregula-tion and awareness to some extent inmany patients (176). Hence, patients withone or more episodes of severe hypogly-cemia may benefit from at least short-term relaxation of glycemic targets.

K. 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, life-threatening conditionsthat require immediate medical care toprevent complications and death. Anycondition leading to deterioration in gly-cemic control necessitates more frequentmonitoring of blood glucose and (in ke-tosis-prone patients) urine or blood ke-tones. Marked hyperglycemia requirestemporary adjustment of the treatmentprogram and, if accompanied by ketosis,vomiting, or alteration in level of con-sciousness, immediate interaction withthe diabetes care team. The patient treatedwith noninsulin therapies or MNT alonemay temporarily require insulin. Ade-quate fluid and caloric intake must be as-sured. Infection or dehydration are 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, seeVIII.A. Diabetes care in the hospital. Forfurther information on management ofDKA or nonketotic hyperosmolar state,refer to the ADA consensus statement onhyperglycemic crises (172).

L. Bariatric surgery

Recommendations● Bariatric surgery may be considered for

adults with BMI �35 kg/m2 and type 2diabetes, especially if the diabetes or as-sociated comorbidities are difficult tocontrol with lifestyle and pharmaco-logic therapy. (B)

● Patients with type 2 diabetes who haveundergone bariatric surgery need life-long lifestyle support and medicalmonitoring. (E)

● Although small trials have shown gly-cemic benefit of bariatric surgery in pa-tients with type 2 diabetes and BMI of30–35 kg/m2, there is currently insuf-ficient evidence to generally recom-mend surgery in patients with BMI �35kg/m2 outside of a research protocol.(E)

● The long- t e rm benefit s , cos t -effectiveness, and risks of bariatric sur-gery in individuals with type 2 diabetesshould be studied in well-designedcontrolled trials with optimal medical

and lifestyle therapy as the comparator.(E)

Gastric reduction surgery, either gastricbanding or procedures that involve by-passing, transposing, or resecting sectionsof the small intestine, when part of a com-prehensive team approach, can be an ef-fective weight loss treatment for severeobesity, and national guidelines supportits consideration for people with type 2diabetes who have BMI exceeding 35 kg/m2. Bariatric surgery has been shown tolead to near- or complete normalization ofglycemia in �55–95% of patients withtype 2 diabetes, depending on the surgicalprocedure. A meta-analysis of studies ofbariatric surgery involving 3,188 patientswith diabetes reported that 78% had re-mission of diabetes (normalization ofblood glucose levels in the absence ofmedications), and that the remission rateswere sustained in studies that had fol-low-up exceeding 2 years (177). Remis-sion rates tend to be lower withprocedures that only constrict the stom-ach, and higher with those that bypassportions of the small intestine. Addition-ally, there is a suggestion that intestinalbypass procedures may have glycemic ef-fects that are independent of their effectson weight, perhaps involving the incretinaxis.

One randomized controlled trialcompared adjustable gastric banding to“best available” medical and lifestyle ther-apy in subjects with type 2 diabetes diag-nosed less than 2 years be forerandomization and BMI 30 – 40 kg/m2

(178). In this trial, 73% of surgicallytreated patients achieved “remission” oftheir diabetes, compared with 13% ofthose treated medically. The latter grouplost only 1.7% of body weight, suggestingthat their therapy was not optimal. Over-all the trial had 60 subjects, and only 13had a BMI under 35 kg/m2, making it dif-ficult to generalize these results widely todiabetic patients who are less severelyobese or with longer duration of diabetes.In a more recent study involving 110 pa-tients with type 2 diabetes and a meanBMI of 47 kg/m2, Roux-en-Y gastric by-pass resulted in a mean loss of excessweight of 63% at 1 year and 84% at 2years (179).

Bariatric surgery is costly in the shortterm and has some risks. Rates of morbid-ity and mortality directly related to thesurgery have been reduced considerablyin recent years, with 30-day mortalityrates now 0.28%, similar to those of lapa-



roscopic cholecystectomy (180). Longer-term concerns include vitamin andmineral deficiencies, osteoporosis, andrare but often severe hypoglycemia frominsulin hypersecretion. Cohort studies at-tempting to match subjects suggest thatthe procedure may reduce longer-termmortality rates (181), and it is reasonableto postulate that there may be recoupingof costs over the long run. Recent retro-spective analyses and modeling studiessuggest that these procedures may be costeffective, when one considers reductionin subsequent health care costs (182–184). However, studies of the mecha-nisms of glycemic improvement andlong-term benefits and risks of bariatricsurgery in individuals with type 2 diabe-tes, especially those who are not severelyobese, will require well-designed clinicaltrials, with optimal medical and lifestyletherapy of diabetes and cardiovascularrisk factors as the comparator.

M. Immunization

Recommendations● Annually provide an influenza vaccine

to all diabetic patients at least 6 monthsof age. (C)

● Administer pneumococcal polysaccha-ride vaccine to all diabetic patients �2years of age. A one-time revaccination isrecommended for individuals �64years of age previously immunizedwhen they were �65 years of age if thevaccine was administered �5 yearsago. Other indications for repeat vacci-nation include nephrotic syndrome,chronic renal disease, and other immu-nocompromised states, such as aftertransplantation. (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% (185).

Safe and effective vaccines are avail-able that can greatly reduce the risk ofserious complications from these diseases(186,187). In a case-control series, influ-enza vaccine was shown to reduce diabe-tes-related hospital admission by as muchas 79% during flu epidemics (186). 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 (CDC) AdvisoryCommittee on Immunization Practicesrecommends influenza and pneumococ-cal vaccines for all individuals with diabe-tes (http://www.cdc.gov/vaccines/recs/).

VI. PREVENTION ANDMANAGEMENT OFDIABETES COMPLICATIONS

A. CVDCVD is the major cause of morbidity andmortality for individuals with diabetes,and 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 individual cardiovas-cular risk factors in preventing or slowingCVD in people with diabetes. Large ben-efits are seen when multiple risk factorsare addressed globally (188,189). Risk forcoronary heart disease (CHD) and forCVD in general can be estimated usingmultivariable risk factor approaches, andsuch a strategy may be desirable to under-take in adult patients prior to institutingpreventive therapy.

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● A goal systolic blood pressure �130

mmHg is appropriate for most patientswith diabetes. (C)

● Based on patient characteristics and re-sponse to therapy, higher or lower sys-tolic blood pressure targets may beappropriate. (B)

● 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)

● Lifestyle therapy for hypertension con-sists of: weight loss, if overweight; Di-etary Approaches to Stop Hypertension(DASH)-style dietary pattern includingreducing sodium and increasing potas-sium intake; moderation of alcohol in-take; and increased physical activity.(B)

● Pharmacologic therapy for patientswith diabetes and hypertension shouldbe with a regimen that includes eitheran ACE inhibitor or an ARB. If one classis not tolerated, the other should besubstituted. If needed to achieve bloodpressure targets, a thiazide diureticshould be added to those with an esti-mated GFR (eGFR) (see below) �30ml/min/1.73 m2 and a loop diuretic forthose with an eGFR �30 ml/min/1.73m2. (C)

● 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 monitored. (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)

Position Statement


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 be done by a trained individ-ual and should follow the guidelinesestablished for nondiabetic individuals:measurement in the seated position, withfeet on the floor and arm supported atheart level, after 5 min of rest. Cuff sizeshould be appropriate for the upper armcircumference. Elevated values should beconfirmed on a separate day. Because ofthe clear synergistic risks of hypertensionand diabetes, the diagnostic cut-off for adiagnosis of hypertension is lower in peo-ple with diabetes (blood pressure �130/80) than those without diabetes (bloodpressure 140/90 mmHg) (190).

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(191,192). However, the preponderanceof the clear evidence of benefits of treat-ment of hypertension in people with dia-betes is based on office measurements.

Treatment goalsEpidemiologic analyses show that bloodpressure values �115/75 mmHg are asso-ciated with increased cardiovascularevent rates and mortality in individualswith diabetes (190,193,194). Random-ized clinical trials have demonstrated thebenefit (reduction in CHD events, stroke,and nephropathy) of lowering bloodpressure to �140 mmHg systolic and�80 mmHg diastolic in individuals withdiabetes (190,195–197). The ACCORDtrial examined whether lowering bloodpressure to a systolic �120 mmHg pro-vides greater cardiovascular protectionthan a systolic blood pressure level of130–140 mmHg in patients with type 2diabetes at high risk for CVD (198). Theblood pressure achieved was 119/64

mmHg in the intensive group and 133/70mmHg in the standard group; the differ-ence achieved was attained with an aver-age of 3.4 medications per participant inthe intensive group and 2.1 in the stan-dard therapy group. The primary out-come was a composite of nonfatal MI,nonfatal stroke, and CVD death; the haz-ard ratio for the primary end point in theintensive group was 0.88 (95% CI 0.73–1.06; P � 0.20). Of the prespecified sec-ondary end points, only stroke andnonfatal stroke were statistically signifi-cantly reduced by intensive blood pres-sure treatment, with a hazard ratio of 0.59(95% CI 0.39–0.89, P � 0.01) and 0.63(95% CI 0.41–0.96, P � 0.03), respec-tively. If this finding is real, the numberneeded to treat to prevent one stroke overthe course of 5 years with intensive bloodpressure management is 89.

In predefined subgroup analyses,there was a suggestion of heterogeneity(P � 0.08) based on whether participantswere randomized to standard or intensiveglycemia intervention. In those random-ized to standard glycemic control, theevent rate for the primary end point was1.89 per year in the intensive blood pres-sure arm and 2.47 in the standard bloodpressure arm, while the respective rates inthe intensive glycemia arm were 1.85 and1.73. If this observation is true, it suggeststhat intensive management to a systolicblood pressure target of �120 mmHgmay be of benefit in those who are nottargeting an A1C of �6% and/or that thebenefit of intensive blood pressure man-agement is diminished by more intensiveglycemia management targeting an A1Cof �6%.

Other recent randomized trial datainclude those from ADVANCE, in whichtreatment with an angiotensin-convertingenzyme inhibitor and a thiazide-type di-uretic reduced the rate of death but notthe composite macrovascular outcome.However, the ADVANCE trial had nospecified targets for the randomized com-parison, and the mean systolic bloodpressure in the intensive group (135mmHg) was not as low as the mean sys-tolic blood pressure in the ACCORD stan-dard therapy group (199). A post hocanalysis of blood pressure control in6,400 patients with diabetes and CADenrolled in the International Verapamil-Trandolapril (INVEST) trial demonstratedthat “tight control” (�130 mmHg) wasnot associated with improved CV out-comes compared with “usual care” (130–140 mmHg) (200).

Only the ACCORD blood pressuretrial formally has examined treatment tar-gets �130 mmHg in diabetes. It is possi-ble that lowering systolic blood pressurefrom the low-130s to less than 120 mmHgdoes not further reduce coronary eventsor death, and that most of the benefit fromlowering blood pressure is achieved bytargeting a goal of �140 mmHg. How-ever, this has not been formally assessed.

The absence of significant harm, thetrends toward benefit in stroke, and thepotential heterogeneity with respect to in-tensive glycemia management suggeststhat previously recommended targets arereasonable pending further analyses andresults. Systolic blood pressure targetsmore or less stringent than �130 mmHgmay be appropriate for individual pa-tients, based on response to therapy,medication tolerance, and individualcharacteristics, keeping in mind that mostanalyses have suggested that outcomesare worse if the systolic blood pressure is�140 mmHg.

Treatment strategiesAlthough there are no well-controlledstudies of diet and exercise in the treat-ment of hypertension in individuals withdiabetes, the Dietary Approaches toStop Hypertension (DASH) study innondiabetic individuals has shown anti-hypertensive effects similar to pharmaco-logic monotherapy. Lifestyle therapyconsists of reducing sodium intake (to�1,500 mg/day) and excess body weight;increasing consumption of fruits, vegeta-bles (8 –10 servings/day), and low-fatdairy products (2–3 servings/day); avoid-ing excessive alcohol consumption (nomore than 2 servings/day in men and nomore than 1 serving/day in women)(201); and increasing activity levels(190). These nonpharmacological strate-gies may also positively affect glycemiaand lipid control. Their effects on cardio-vascular events have not been established.An initial trial of nonpharmacologic ther-apy may be reasonable in diabetic individ-uals with mild hypertension (systolicblood pressure 130–139 mmHg or dia-stolic blood pressure 80–89 mmHg). Ifsystolic blood pressure is �140 mmHgand/or diastolic is �90 mmHg at the timeof diagnosis, pharmacologic therapyshould be initiated along with nonphar-macologic therapy (190).

Lowering of blood pressure with reg-imens based on a variety of antihyperten-sive drugs, including ACE inhibitors,ARBs, �-blockers, diuretics, and calcium



channel 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 (202–204). However, a variety of other studieshave shown no specific advantage to ACEinhibitors as initial treatment of hyperten-sion in the general hypertensive popula-tion, but rather an advantage oncardiovascular outcomes of initial therapywith low-dose thiazide diuret ics(190,205,206).

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(207). In patients with congestive heartfailure (CHF), including diabetic sub-groups, ARBs have been shown to reducemajor CVD outcomes (208–211), and intype 2 patients with significant nephrop-athy, ARBs were superior to calciumchannel blockers for reducing heart fail-ure (212). Though evidence for distinctadvantages of RAS inhibitors on CVD out-comes in diabetes remains conflicting(195,206), the high CVD risks associatedwith diabetes, and the high prevalence ofundiagnosed CVD, may still favor recom-mendations for their use as first-line hy-pertension therapy in people withdiabetes (190). Recently, the blood pres-sure arm of the ADVANCE trial demon-strated that routine administration of afixed combination of the ACE inhibitorperindopril and the diuretic indapamidesignificantly reduced combined micro-vascular and macrovascular outcomes, aswell as CVD and total mortality. The im-proved outcomes could also have beendue to lower achieved blood pressure inthe perindopril-indapamide arm (199).In addition, the Avoiding CardiovascularEvents through Combination Therapy inPatients Living with Systolic Hyperten-sion (ACCOMPLISH) trial showed a de-crease in morbidity and mortality in thosereceiving benazapril and amlodipine ver-sus benazapril and hydrochlorothiazide.The compelling benefits of RAS inhibitorsin diabetic patients with albuminuria orrenal insufficiency provide additional ra-tionale for use of these agents (see VI.B.Nephropathy screening and treatment).

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(190). If blood pressure is refractory tooptimal doses of at least three antihyper-tensive agents of different classifications,one of which should be a diuretic, clini-cians should consider an evaluation forsecondary forms of hypertension.

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 can cause fetal damage. Anti-hypertensive drugs known to be effectiveand safe in pregnancy include methyl-dopa, labetalol, diltiazem, clonidine, andprazosin. Chronic diuretic use duringpregnancy has been associated with re-stricted maternal plasma volume, whichmight reduce uteroplacental perfusion(213).

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; increase of omega-3fatty acids, viscous fiber, and plantstanols/sterols; 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 age 40

years and have one or more otherCVD risk factors. (A)

● For patients at lower risk than above(e.g., without overt CVD and under age

40 years), statin therapy should be con-sidered in addition to lifestyle therapy ifLDL cholesterol remains above 100mg/dl or in those with multiple CVDrisk 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 (1.8mmol/l), using a high dose of a statin, isan option. (B)

● If drug-treated patients do not reach theabove targets on maximal tolerated sta-tin therapy, a reduction in LDL choles-terol of �30–40% from baseline is analternative therapeutic goal. (A)

● Triglyceride 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 de-sirable. However, LDL cholesterol–targeted statin therapy remains thepreferred strategy. (C)

● If targets are not reached on maximallytolerated doses of statins, combinationtherapy using statins and other lipid-lowering agents may be considered toachieve lipid targets but has not beenevaluated in outcome studies for eitherCVD outcomes or safety. (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,contributing to their high risk of CVD.For the past decade or more, multipleclinical trials demonstrated significant ef-fects of pharmacologic (primarily statin)therapy on CVD outcomes in subjectswith CHD and for primary CVD preven-tion (214). Sub-analyses of diabetic sub-groups of larger trials (215–219) andtrials specifically in subjects with diabetes(220,221) showed significant primaryand secondary prevention of CVDevents � CHD deaths in diabetic popula-tions. As shown in Table 11, and similarto findings in nondiabetic subjects, re-duction in “hard” CVD outcomes (CHDdeath and nonfatal MI) can be moreclearly seen in diabetic subjects with highbaseline CVD risk (known CVD and/orvery high LDL cholesterol levels), butoverall the benefits of statin therapy inpeople with diabetes at moderate or highrisk for CVD are convincing.

Low levels of HDL cholesterol, oftenassociated with elevated triglyceride lev-

Position Statement


els, are the most prevalent pattern of dys-lipidemia in persons with type 2 diabetes.However, the evidence base for drugs thattarget these lipid fractions is significantlyless robust than that for statin therapy(222). Nicotinic acid has been shown toreduce CVD outcomes (223), althoughthe study was done in a nondiabetic co-hort. Gemfibrozil has been shown to de-crease rates of CVD events in subjectswithout diabetes (224,225) and in the di-abetic subgroup in one of the larger trials(224). However, in a large trial specific todiabetic patients, fenofibrate failed to re-duce overall cardiovascular outcomes(226).

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)(227). 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 and increases in omega-3fatty acids, viscous fiber (such as in oats,legumes, citrus), and plant stanols/sterols. Glycemic control can also benefi-cially modify plasma lipid levels,particularly in patients with very hightriglycerides and poor glycemic control.

In those with clinical CVD or over age40 years with other CVD risk factors,pharmacological treatment should beadded to lifestyle therapy regardless ofbaseline lipid levels. Statins are the drugsof choice for LDL cholesterol lowering.

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 age 40 years or fortype 1 patients of any age. In the HeartProtection Study (lower age limit 40years), the subgroup of 600 patients withtype 1 diabetes had a proportionately sim-ilar reduction in risk as patients with type2 diabetes, although not statistically sig-nificant (216). Although the data are notdefinitive, consideration should be givento similar lipid-lowering goals in type 1

diabetic patients as in type 2 diabetic pa-tients, particularly if they have other car-diovascular risk factors.

Alternative LDL cholesterol goalsVirtually all trials of statins and CVD out-comes tested specific doses of statinsagainst placebo, other doses of statin, orother statins, rather than aiming for spe-cific LDL cholesterol goals (228). As canbe seen in Table 11, placebo-controlledtrials generally achieved LDL cholesterolreductions of 30 – 40% from baseline.Hence, LDL cholesterol lowering of thismagnitude is an acceptable outcome forpatients who cannot reach LDL choles-terol goals due to severe baseline eleva-t ions in LDL choles tero l and/orintolerance of maximal, or any, statindoses. Additionally for those with base-line LDL cholesterol minimally above 100mg/dl, prescribing statin therapy to lowerLDL cholesterol about 30 – 40% frombaseline is probably more effective thanprescribing just enough to get LDL cho-lesterol slightly below 100 mg/dl.

Recent clinical trials in high-risk pa-tients, such as those with acute coronarysyndromes or previous cardiovascularevents (229 –231), have demonstratedthat more aggressive therapy with highdoses of statins to achieve an LDL choles-terol of �70 mg/dl led to a significant re-

Table 11—Reduction in 10-year risk of major CVD endpoints (CHD death/non-fatal MI) in major statin trials, or substudies of major trials,in diabetic subjects (n � 16,032)

Study (ref.) CVDStatin dose and

comparatorRisk

reduction (%)Relative risk

reduction (%)Absolute riskreduction (%)

LDL cholesterolreduction (mg/dl)

LDL cholesterolreduction (%)

4S-DM (215) 2° Simvastatin 20–40 mgvs. placebo

85.7 to 43.2 50 42.5 186 to 119 36

ASPEN 2° (220) 2° Atorvastatin 10 mg vs.placebo

39.5 to 24.5 34 15 112 to 79 29

HPS-DM (216) 2° Simvastatin 40 mg vs.placebo

43.8 to 36.3 17 7.5 123 to 84 31

CARE-DM (217) 2° Pravastatin 40 mg vs.placebo

40.8 to 35.4 13 5.4 136 to 99 27

TNT-DM (218) 2° Atorvastatin 80 mg vs.10 mg

26.3 to 21.6 18 4.7 99 to 77 22

HPS-DM (216) 1° Simvastatin 40 mg vs.placebo

17.5 to 11.5 34 6.0 124 to 86 31

CARDS (221) 1° Atorvastatin 10 mg vs.placebo

11.5 to 7.5 35 4 118 to 71 40

ASPEN 1° (220) 1° Atorvastatin 10 mg vs.placebo

9.8 to 7.9 19 1.9 114 to 80 30

ASCOT-DM (219) 1° Atorvastatin 10 mg vs.placebo

11.1 to 10.2 8 0.9 125 to 82 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 endpoints (CHD death/nonfatal MI) are listed for comparison between studies. Correlation between 10-year CVDrisk of the control group and the absolute risk reduction with statin therapy is highly significant (P � 0.0007). Analyses provided by Craig Williams, PharmD, OregonHealth & Science University, 2007.



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 (232).

In individual patients, LDL choles-terol lowering with statins is highly vari-able, and this variable response is poorlyunderstood (233). Reduction of CVDevents with statins correlates very closelywith LDL cholesterol lowering (214).When maximally tolerated doses of st-atins fail to significantly lower LDL cho-lesterol (�30% reduction from patientsbaseline), the primary aim of combinationtherapy should be to achieve additionalLDL cholesterol lowering. Niacin, fenofi-brate, ezetimibe, and bile acid seques-trants all offer additional LDL cholesterollowering. The evidence that combinationtherapy provides a significant incrementin CVD risk reduction over statin therapyalone is still elusive.

In 2008, a consensus panel convenedby the American Diabetes Association andthe American College of Cardiology rec-ommended a greater focus on non-HDLcholesterol and apo lipoprotein B (apo B)in patients who are likely to have smallLDL particles, such as people with diabe-tes (234). The consensus panel suggestedthat for statin-treated patients in whomthe LDL cholesterol goal would be �70mg/dl (non-HDL cholesterol �100 mg/dl), apo B should be measured and treatedto �80 mg/dl. For patients on statins withan LDL cholesterol goal of �100 mg/dl(non-HDL cholesterol �130 mg/dl), apoB should be measured and treated to �90mg/dl.

Treatment of other lipoproteinfractions or targetsSevere hypertriglyceridemia may warrantimmediate therapy of this abnormalitywith lifestyle and usually pharmacologictherapy (fibric acid derivative, niacin, orfish oil) to reduce the risk of acute pan-creatitis. In the absence of severe hyper-triglyceridemia, therapy targeting HDLcholesterol or triglycerides has intuitiveappeal but lacks the evidence base of sta-tin therapy. If the HDL cholesterol is �40mg/dl and the LDL cholesterol between100 and 129 mg/dl, gemfibrozil or niacinmight be used, especially if a patient isintolerant to statins. Niacin is the mosteffective drug for raising HDL cholesterol.It can significantly increase blood glucoseat high doses, but recent studies demon-strate that at modest doses (750–2,000mg/day), significant improvements inLDL cholesterol, HDL cholesterol, and

triglyceride levels are accompanied byonly modest changes in glucose that aregenerally amenable to adjustment of dia-betes therapy (235,236).

Combination therapyCombination therapy, with a statin and afibrate or statin and niacin, may be effica-cious for treatment for all three lipid frac-tions, but this combination is associatedwith 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 (237). In therecent ACCORD study, the combinationof fenofibrate and simvastatin did not re-duce the rate of fatal cardiovascularevents, nonfatal myocardial infarction, ornonfatal stroke, as compared with simva-statin alone, in patients with type 2 dia-betes who were at high risk for CVD.However, prespecified subgroup analysessuggested heterogeneity in treatment ef-fects according to sex, with a benefit formen and possible harm for women, and apossible benefit of combination therapyfor patients with both triglyceride level�204 mg/dl and HDL cholesterol level�34 mg/dl (238). Other ongoing trialsmay provide much-needed evidence forthe effects of combination therapy on car-diovascular outcomes.

Table 12 summarizes common treatmentgoals for A1C, blood pressure, and HDLcholesterol.

3. Antiplatelet agents

Recommendations● Consider aspirin therapy (75–162 mg/

day) as a primary prevention strategy inthose with type 1 or type 2 diabetes atincreased cardiovascular risk (10-yearrisk �10%). This includes most men�50 years of age or women �60 yearsof age who have at least one additionalmajor risk factor (family history ofCVD, hypertension, smoking, dyslipi-demia, or albuminuria). (C)

● Aspirin should not be recommendedfor CVD prevention for adults with di-abetes at low CVD risk (10-year CVDrisk �5%, such as in men �50 andwomen �60 years of age with no majoradditional CVD risk factors), since thepotential adverse effects from bleedinglikely offset the potential benefits. (C)

● In patients in these age-groups with

multiple other risk factors (e.g., 10-yearrisk 5–10%), clinical judgment is re-quired. (E)

● Use aspirin therapy (75–162 mg/day)as a secondary prevention strategy inthose with diabetes with a history ofCVD. (A)

● For patients with CVD and docu-mented aspirin allergy, clopidogrel (75mg/day) should be used. (B)

● Combination therapy with ASA (75–162 mg/day) and clopidogrel (75 mg/day) is reasonable for up to a year afteran acute coronary syndrome. (B)

ADA and the American Heart Association(AHA) have, in the past, jointly recom-mended that low-dose aspirin therapy beused as a primary prevention strategy inthose with diabetes at increased cardio-vascular risk, including those who areover 40 years of age or those with addi-tional risk factors (family history of CVD,hypertension, smoking, dyslipidemia, oralbuminuria) (188). These recommenda-tions were derived from several older tri-als that included small numbers ofpatients with diabetes.

Aspirin has been shown to be effec-tive in reducing cardiovascular morbidityand mortality in high-risk patients withprevious myocardial infarction or stroke(secondary prevention). Its net benefit inprimary prevention among patients withno previous cardiovascular events is morecontroversial, both for patients with andwithout a history of diabetes (239). Tworecent randomized controlled trials of as-pirin specifically in patients with diabetesfailed to show a significant reduction inCVD end points, raising further questionsabout the efficacy of aspirin for primary

Table 12—Summary of recommendationsfor glycemic blood pressure and lipid controlfor most adults with diabetes

A1C �7.0%*Blood pressure �130/80 mmHg†Lipids

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

*More or less stringent glycemic goals may be ap-propriate for individual patients. Goals should beindividualized based on: duration of diabetes, age/life expectancy, comorbid conditions, known CVDor advanced microvascular complications, hypogly-cemia unawareness, and individual patient consid-erations. †Based on patient characteristics andresponse to therapy, higher or lower systolic bloodpressure targets may be appropriate. ‡In individualswith overt CVD, a lower LDL cholesterol goal of�70 mg/dl (1.8 mmol/l), using a high dose of astatin, is an option.

Position Statement


prevention in people with diabetes(240,241).

The Anti-thrombotic Trialists’ (ATT)collaborators recently published an indi-vidual patient-level meta-analysis of thesix large trials of aspirin for primary pre-vention in the general population. Thesetrials collectively enrolled over 95,000participants, including almost 4,000 withdiabetes. Overall, they found that aspirinreduced the risk of vascular events by12% (RR 0.88 [95% CI 0.82– 0.94]). Thelargest reduction was for nonfatal myo-cardial infarction with little effect on CHDdeath (RR 0.95 [95% CI 0.78–1.15]) ortotal stroke. There was some evidence of adifference in aspirin effect by sex. Aspirinsignificantly reduced CHD events in menbut not in women. Conversely, aspirinhad no effect on stroke in men but signif-icantly reduced stroke in women. Nota-bly, sex differences in aspirin’s effectshave not been observed in studies of sec-ondary prevention (239). In the six trialsexamined by the ATT collaborators, theeffects of aspirin on major vascular eventswere similar for patients with or withoutdiabetes: RR 0.88 (95% CI 0.67–1.15)and 0.87 (0.79–0.96), respectively. TheCI was wider for those with diabetes be-cause of their smaller number.

Based on the currently available evi-dence, aspirin appears to have a modesteffect on ischemic vascular events withthe absolute decrease in events dependingon the underlying CVD risk. The mainadverse effects appear to be an increasedrisk of gastrointestinal bleeding. The ex-cess risk may be as high as 1–5 per 1,000per year in real-world settings. In adultswith CVD risk greater than 1% per year,the number of CVD events prevented willbe similar to or greater than the number ofepisodes of bleeding induced, althoughthese complications do not have equal ef-fects on long-term health (242).

In 2010, a position statement of theADA, AHA, and American College of Car-diology Foundation (ACCF) updatedprior joint recommendations for primaryprevention (243). Low dose (75–162 mg/day) aspirin use for primary prevention isreasonable for adults with diabetes and noprevious history of vascular disease whoare at increased CVD risk (10-year risk ofCVD events over 10%) and who are not atincreased risk for bleeding. This generallyincludes most men over age 50 years andwomen over age 60 years who also haveone or more of the following major riskfactors: smoking, hypertension, dyslipi-

demia, family history of premature CVD,and albuminuria.

However, aspirin is no longer recom-mended for those at low CVD risk(women under age 60 years and men un-der age 50 years with no major CVD riskfactors; 10-year CVD risk under 5%) asthe low benefit is likely to be outweighedby the risks of significant bleeding. Clin-ical judgment should be used for those atintermediate risk (younger patients withone or more risk factors, or older patientswith no risk factors; those with 10-yearCVD risk of 5–10%) until further researchis available. Use of aspirin in patients un-der the age of 21 years is contraindicateddue to the associated risk of Reye’s syn-drome.

Average daily dosages used in mostclinical trials involving patients with dia-betes ranged from 50 to 650 mg but weremostly in the range of 100 to 325 mg/day.There is little evidence to support any spe-cific dose, but using the lowest possibledosage may help reduce side effects(244). Although platelets from patientswith diabetes have altered function, it isunclear what, if any, impact that findinghas on the required dose of aspirin forcardioprotective effects in the patientwith diabetes. Many alternate pathwaysfor platelet activation exist that are inde-pendent of thromboxane A2 and thus notsensitive to the effects of aspirin (245).Therefore, while “aspirin resistance” ap-pears higher in the diabetic patients whenmeasured by a variety of ex vivo and invitro methods (platelet aggrenometry,measurement of thromboxane B2), theseobservations alone are insufficient to em-pirically recommend higher doses of as-pirin be used in the diabetic patient at thistime.

Clopidogrel has been demonstratedto reduce CVD events in diabetic individ-uals (246). It is recommended as adjunc-tive therapy in the first year after an acutecoronary syndrome or as alternative ther-apy in aspirin-intolerant patients.

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)

A large body of evidence from epidemio-logical, case-control, and cohort studiesprovides convincing documentation ofthe causal link between cigarette smoking

and health risks. Much of the work doc-umenting the impact of smoking onhealth did not separately discuss resultson subsets of individuals with diabetes,but suggests that the identified risks are atleast equivalent to those found in the gen-eral population. Other studies of individ-ua l s w i th d i abe t e s cons i s t en t l ydemonstrate that smokers have a height-ened risk of CVD, premature death, andincreased rate of microvascular complica-tions of diabetes. Smoking may have arole in the development of type 2 diabe-tes.

The routine and thorough assess-ment of tobacco use is important as ameans of preventing smoking or en-couraging cessation. A number of largerandomized clinical trials have demon-strated the efficacy and cost-effective-ness of brief counseling in smokingcessation, including the use of quitlines, in the reduction of tobacco use.For the patient motivated to quit, theaddition of pharmacological therapy tocounseling is more effective than eithertreatment alone. Special considerationsshould include assessment of level ofnicotine dependence, which is associ-ated with difficulty in quitting and re-lapse (247).

5. CHD screening and treatment

Recommendations

Screening● In asymptomatic patients, routine

screening for CAD is not recom-mended, as it does not improve out-comes as long as CVD risk factors aretreated. (A)

Treatment● In patients with known CVD, ACE in-

hibitor (C) and aspirin and statin ther-apy (A) (if not contraindicated) shouldbe used to reduce the risk of cardiovas-cular events.

● In patients with a prior myocardial in-farction, �-blockers should be contin-ued for at least 2 years after the event(B).

● Longer term use of �-blockers in theabsence of hypertension is reasonable ifwell tolerated, but data are lacking. (E)

● Avoid TZD treatment in patients withsymptomatic heart failure. (C)

● Metformin may be used in patients withstable CHF if renal function is normal.It should be avoided in unstable or hos-pitalized patients with CHF. (C)



Screening for CAD is reviewed in a re-cently updated consensus statement(154). To identify the presence of CADin diabetic patients without clear orsuggestive symptoms, a risk factor–based approach to the initial diagnosticevaluation and subsequent follow-uphas intuitive appeal. However, recentstudies concluded that using this ap-proach fails to identify which patientswith type 2 diabetes will have silentischemia on screening tests (159,248).

Candidates for cardiac testing in-clude those with 1) typical or atypicalcardiac symptoms and 2) an abnormalresting ECG. The screening of asymp-tomatic patients remains controversial,especially as intensive medical therapy,indicated in diabetic patients at highrisk for CVD, has an increasing evidencebase for providing equal outcomes toinvasive revascularization, including indiabetic patients (249,250). There isalso some evidence that silent myocar-dial ischemia may reverse over time,adding to the controversy concerningaggressive screening strategies (251).Finally, a recent randomized observa-tional trial demonstrated no clinicalbenefit to routine screening of asymp-tomatic patients with type 2 diabetesand normal ECGs (252). Despite abnor-mal myocardial perfusion imaging inmore than one in five patients, cardiacoutcomes were essentially equal (andvery low) in screened versus un-screened patients. Accordingly, theoverall effectiveness, especially thecost-effectiveness, of such an indiscrim-inate screening strategy is now ques-tioned.

Newer noninvasive CAD screeningmethods, such as computed tomogra-phy (CT) and CT angiography havegained in popularity. These tests inferthe presence of coronary atherosclerosisby measuring the amount of calcium incoronary arteries and, in some circum-stances, by direct visualization of lumi-nal stenoses. Although asymptomaticdiabetic patients found to have a highercoronary disease burden have more fu-ture cardiac events (253–255), the roleof these tests beyond risk stratificationis not clear. Their routine use leads toradiation exposure and may result inunnecessary invasive testing such ascoronary angiography and revascular-ization procedures. The ultimate bal-ance of benefit, cost, and risks of suchan approach in asymptomatic patientsremains controversial, particularly in

the modern setting of aggressive CVDrisk factor control.

In all patients with diabetes, cardio-vascular risk factors should be assessedat least annually. These risk factors in-clude dyslipidemia, hypertension,smoking, a positive family history ofpremature coronary disease, and thepresence of micro- or macroalbumin-uria. Abnormal risk factors should betreated as described elsewhere in theseguidelines. Patients at increased CHDrisk should receive aspirin and a statinand ACE inhibitor or ARB therapy if hy-pertensive, unless there are contraindi-cations to a particular drug class. Whileclear benefit exists for ACE inhibitorand ARB therapy in patients with ne-phropathy or hypertension, the benefitsin patients with CVD in the absence ofthese conditions is less clear, especiallywhen LDL cholesterol is concomitantlycontrolled (256,257).

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 5 yearsand in all type 2 diabetic patients start-ing 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 wt1 � day1 in individualswith diabetes and the earlier stages ofCKD and to 0.8 g � kg body wt1 �day1 in the later stages of CKD mayimprove measures of renal function(urine albumin excretion rate, GFR)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)

● When eGFR �60 ml/min/1.73 m2,

evaluate and manage potential compli-cations of CKD. (E)

● Consider referral to a physician experi-enced in the care of kidney diseasewhen there is uncertainty about the eti-ology of kidney disease (heavy protein-uria, active urine sediment, absence ofretinopathy, rapid decline in GFR), dif-ficult management issues, or advancedkidney 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 (258,259).Patients with microalbuminuria whoprogress to macroalbuminuria (300mg/24 h) are likely to progress to ESRD(260,261). However, a number of inter-ventions have been demonstrated to re-

Position Statement


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 (262,263) and type 2 (55,56)diabetes. The UKPDS provided strong ev-idence that control of blood pressure canreduce the development of nephropathy(195). 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 in pa-tients with macroalbuminuria (264 –266) . In type 2 diabetes wi thhypertension and normoalbuminuria,RAS inhibition has been demonstrated todelay onset of microalbuminuria (267).

In addition, ACE inhibitors have beenshown to reduce major CVD outcomes(i.e., myocardial infarction, stroke, death)in patients with diabetes (207), thus fur-ther supporting the use of these agents inpatients with microalbuminuria, a CVDrisk factor. ARBs do not prevent mi-croalbuminuria in normotensive patientswith type 1 or type 2 diabetes (268,269);however, ARBs have been shown to re-duce the rate of progression from micro-to macroalbuminuria as well as ESRD inpatients with type 2 diabetes (270–272).Some evidence suggests that ARBs have asmaller magnitude of rise in potassiumcompared with ACE inhibitors in peoplewith nephropathy (273,274). Combina-tions of drugs that block the renin-angiotensin-aldosterone system (e.g., anACE inhibitor plus an ARB, a mineralo-corticoid antagonist, or a direct renin in-hibitor) have been shown to provideadditional lowering of albuminuria (275–278). However, the long-term effects ofsuch combinations on renal or cardiovas-cular outcomes have not yet been evalu-ated in clinical trials, and they areassociated with increased risk for hyper-kalemia.

Other drugs, such as diuretics, cal-cium channel blockers, and �-blockersshould be used as additional therapy tofurther lower blood pressure in patientsalready treated with ACE inhibitors orARBs (212), or as alternate therapy in the

rare individual unable to tolerate ACE in-hibitors or ARBs.

Studies in patients with varying stagesof nephropathy have shown that proteinrestriction of dietary protein helps slowthe progression of albuminuria, GFR de-cline, and occurrence of ESRD (279 –282). Dietary protein restriction shouldbe considered particularly in patientswhose nephropathy seems to be progress-ing despite optimal glucose and bloodpressure control and use of ACE inhibitorand/or ARBs (282).

Assessment of albuminuria statusand renal functionScreening for microalbuminuria can beperformed by measurement of the albu-min-to-creatinine ratio in a random spotcollection; 24-h or timed collections aremore burdensome and add little to pre-diction or accuracy (283,284). Measure-ment of a spot urine for albumin only,whether by immunoassay or by using adipstick test specific for microalbumin,without simultaneously measuring urinecreatinine, is somewhat less expensive butsusceptible to false-negative and -positivedeterminations as a result of variation inurine concentration due to hydration andother factors.

Abnormalities of albumin excretionare defined in Table 13. 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 crossed

one of these diagnostic thresholds. Exer-cise within 24 h, infection, fever, CHF,marked hyperglycemia, and marked hy-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 14) is primarily based onGFR levels and therefore differs fromother systems, in which staging is basedprimarily on urinary albumin excretion(285). Studies have found decreased GFRin the absence of increased urine albuminexcretion in a substantial percentage ofadults with diabetes (286). Serum creati-nine should therefore be measured at leastannually in all adults with diabetes, re-gardless of the degree of urine albuminexcretion.

Serum creatinine should be used toestimate GFR and to stage the level ofCKD, if present. eGFR is commonly co-reported by laboratories or can be esti-mated using formulae such as theModification of Diet in Renal Disease(MDRD) study equation (287). Recent re-ports have indicated that the MDRD ismore accurate for the diagnosis and strat-ification of CKD in patients with diabetesthan the Cockcroft-Gault formula (288).GFR calculators are available at http://www.nkdep.nih.gov.

The role of continued annual quan-titative assessment of albumin excretionafter diagnosis of microalbuminuria andinstitution of ACE inhibitor or ARBtherapy and blood pressure control isunclear. Continued surveillance can as-sess both response to therapy and pro-gression of disease. Some suggest thatreducing abnormal albuminuria (�30mg/g) to the normal or near-normalrange may improve renal and cardiovas-cular prognosis, but this approach hasnot been formally evaluated in prospec-tive trials.

Table 14—Stages of CKD

Stage DescriptionGFR (ml/min per 1.73 m2

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.284.

Table 13—Definitions of abnormalities in al-bumin excretion

Category

Spot collection(g/mg

creatinine)

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



Complications of kidney disease cor-relate with level of kidney function. Whenthe eGFR is less than 60 ml/min/1.73 m2,screening for complications of CKD is in-dicated (Table 15). Early vaccinationagainst hepatitis B is indicated in patientslikely to progress to end-stage kidney dis-ease.

Consider referral to a physician ex-perienced in the care of kidney diseasewhen there is uncertainty about the eti-ology of kidney disease (heavy protein-uria, active urine sediment, absence ofretinopathy, rapid decline in GFR, re-sistant hypertension), difficult manage-ment issues, or advanced kidneydisease. The threshold for referral mayvary depending on the frequency withwhich a provider encounters diabeticpatients with significant kidney disease.Consultation with a nephrologist whenstage 4 CKD develops has been found toreduce cost, improve quality of care,and keep people off dialysis longer(289). However, nonrenal specialistsshould not delay educating their pa-tients about the progressive nature ofdiabetic kidney disease; the renal pres-ervation benefits of aggressive treat-ment of blood pressure, blood glucose,and hyperlipidemia; and the potentialneed for renal replacement 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 children aged 10 years or

older with type 1 diabetes should havean initial dilated and comprehensiveeye examination by an ophthalmologistor optometrist within 5 years after theonset of diabetes. (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)

● High-quality fundus photographs candetect most clinically significant dia-betic retinopathy. Interpretation of theimages should be performed by atrained eye care provider. While retinalphotography may serve as a screeningtool for retinopathy, it is not a substi-tute for a comprehensive eye exam,which should be performed at least ini-tially and at intervals thereafter as rec-ommended by an eye care professional.(E)

● Women with preexisting diabetes whoare planning a pregnancy or who havebecome pregnant should have a com-prehensive eye examination and shouldbe counseled on the risk of develop-ment and/or progression of diabetic ret-inopathy. Eye examination shouldoccur in the first trimester with closefollow-up throughout pregnancy andfor 1 year postpartum. (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 in

patients 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 doesnot 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 (290), the pres-ence of nephropathy (291), and hyper-tension (292). Intensive diabetesmanagement with the goal of achievingnear normoglycemia has been shown inlarge prospective randomized studies toprevent and/or delay the onset and pro-gression of diabetic retinopathy (47,55,56,64). Lowering blood pressure hasbeen shown to decrease the progressionof retinopathy (195). Several case seriesand a controlled prospective study sug-gest that pregnancy in type 1 diabetic pa-t ients may aggravate ret inopathy

Table 15—Management of CKD in diabetes

GFR (ml/min/1.73 m2) Recommended

All patients Yearly measurement of creatinine, urinary albumin excretion, potassium45–60 Referral to nephrology if possibility for nondiabetic kidney disease exists

(duration type 1 diabetes �10 years, heavy proteinuria, abnormalfindings on renal ultrasound, resistant hypertension, rapid fall inGFR, or active urinary sediment)

Consider need for dose adjustment of medicationsMonitor eGFR every 6 monthsMonitor electrolytes, bicarbonate, hemoglobin, calcium, phosphorus,

parathyroid hormone at least yearlyAssure vitamin D sufficiencyConsider bone density testingReferral for dietary counselling

30–44 Monitor eGFR every 3 monthsMonitor electrolytes, bicarbonate, calcium, phosphorus, parathyroid

hormone, hemoglobin, albumin, weight every 3–6 monthsConsider need for dose adjustment of medications

�30 Referral to nephrologist

Adapted from http://www.kidney.org/professionals/KDOQI/guideline_diabetes/.

Position Statement


(293,294); laser photocoagulation sur-gery can minimize this risk (294).

One of the main motivations forscreening for diabetic retinopathy is theestablished efficacy of laser photocoagu-lation surgery in preventing vision 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 (295) showed that panreti-nal photocoagulation surgery reduced therisk of severe vision loss from PDR from15.9% in untreated eyes to 6.4% intreated eyes, with greatest risk-to-benefitratio in those with baseline disease (discneovascularization or vitreous hemor-rhage).

The ETDRS (296) 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 and in older-onset patients with severe NPDR or less-than-high-risk PDR.

Laser photocoagulation surgery inboth trials was beneficial in reducing therisk of further vision 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, patients with type 1 dia-betes 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 andwho have a significant risk of prevalentDR at time of diabetes diagnosis, shouldhave an initial dilated and comprehensiveeye examination soon after diagnosis. Ex-aminations should be performed by anophthalmologist or optometrist who isknowledgeable and experienced in diag-nosing the presence of diabetic retinopa-thy and is aware of its management.Subsequent examinations for type 1 andtype 2 diabetic patients are generally re-peated annually. Less-frequent exams(every 2–3 years) may be cost effective

after one or more normal eye exams,while examinations will be required morefrequently if retinopathy is progressing(297).

The use of retinal photography withremote reading by experts has great po-tential 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 (298). In-personexams are still necessary when the photosare unacceptable and for follow-up of ab-normalities detected. Photos are not asubstitute for a comprehensive eye exam,which should be performed at least ini-tially and at intervals thereafter as recom-mended by an eye care professional.

Results of eye examinations should bedocumented and transmitted to the refer-ring health care professional. For a de-tailed review of the evidence and furtherdiscussion of diabetic retinopathy, see theADA’s technical review and position state-ment on this subject (297,300).

D. Neuropathy screening andtreatment (301)

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)

● 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 a di-agnos i s o f exc lus ion , complexinvestigations to exclude other conditionsare rarely needed.

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, and 4) autonomic neuropathyand particularly cardiovascular auto-nomic neuropathy is associated with sub-stantial morbidity and even mortality.Specific treatment for the underlyingnerve damage is currently not available,other than improved glycemic control,which may modestly slow progression(63) but not reverse neuronal loss. Effec-tive symptomatic treatments are availablefor some manifestations of DPN and au-tonomic neuropathy.

Diagnosis of neuropathyDistal symmetric polyneuropathy. Pa-tients 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 (301). Importantly, inpatients with neuropathy, particularlywhen severe, causes other than diabetesshould always be considered, such asneurotoxic mediations, heavy metal poi-soning, alcohol abuse, vitamin B12 defi-ciency (especially in those takingmetformin for prolonged periods (302),renal disease, chronic inflammatory de-myelinating neuropathy, inherited neu-ropathies, and vasculitis (303).Diabetic autonomic neuropathy (304).The 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 funct ion, and, potent ia l ly ,autonomic failure in response to hypogly-cemia.

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) or orthostasis (a fall in systolicblood pressure �20 mmHg upon stand-ing without an appropriate heart rate re-sponse); it is also associated withincreased cardiac event rates.

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.

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.

Symptomatic treatmentsDPN. The first step in management of pa-tients with DPN should be to aim for sta-ble and optimal glycemic control.Although controlled trial evidence is lack-ing, several observational studies suggestthat neuropathic symptoms improve notonly with optimization of control, butalso with the avoidance of extreme bloodglucose fluctuations. Patients with painfulDPN may benefit from pharmacologicaltreatment of their symptoms: manyagents have efficacy confirmed in pub-lished randomized controlled trials, sev-eral of which are Food and DrugAdministration (FDA)-approved for themanagement of painful DPN.

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 neuropathy

are described in the ADA statement onneuropathy (301). 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 should include inspection,assessment of foot pulses, and testingfor loss of protective sensation (10-gmonofilament plus testing any one of:vibration using 128-Hz tuning fork,pinprick sensation, ankle reflexes, orvibration perception threshold). (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 those witha history of prior ulcer or amputation.(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-ment of risk factors can prevent or delayadverse outcomes.

The risk of ulcers or amputations isincreased in people who have the follow-ing risk factors:

● Previous amputation● Past foot ulcer history● Peripheral neuropathy● Foot deformity● Peripheral vascular disease

● Visual impairment● Diabetic nephropathy (especially pa-

tients on dialysis)● Poor glycemic control● Cigarette smoking

Many studies have been published pro-posing a range of tests that might usefullyidentify patients at risk of foot ulceration,creating confusion among practitioners asto which screening tests should beadopted in clinical practice. An ADA taskforce was therefore assembled in 2008 toconcisely summarize recent literature inthis area and then recommend whatshould be included in the comprehensivefoot exam for adult patients with diabetes.Their recommendations are summarizedbelow, but clinicians should refer to thetask force report (305) for further detailsand practical descriptions of how to per-form components of the comprehensivefoot examination.

At least annually, all adults with dia-betes should undergo a comprehensivefoot examination to identify high riskconditions. Clinicians should ask abouthistory of previous foot ulceration or am-putation, neuropathic or peripheral vas-cular symptoms, impaired vision, tobaccouse, and foot care practices. A general in-spection of skin integrity and musculo-skeletal deformities should be done in awell lit room. Vascular assessment wouldinclude inspection and assessment ofpedal pulses.

The neurologic exam recommendedis designed to identify loss of protectivesensation (LOPS) rather than early neu-ropathy. The clinical examination to iden-tify LOPS is simple and requires noexpensive equipment. Five simple clinicaltests (use of a 10-g monofilament, vibra-tion testing using a 128-Hz tuning fork,tests of pinprick sensation, ankle reflexassessment, and testing vibration percep-tion threshold with a biothesiometer),each with evidence from well-conductedprospective clinical cohort studies, areconsidered useful in the diagnosis ofLOPS in the diabetic foot. The task forceagrees that any of the five tests listed couldbe used by clinicians to identify LOPS,although ideally two of these should beregularly performed during the screeningexam—normally the 10-g monofilamentand one other test. One or more abnormaltests would suggest LOPS, while at leasttwo normal tests (and no abnormal test)would rule out LOPS. The last test listed,vibration assessment using a biothesiom-eter or similar instrument, is widely used

Position Statement


in the U.S.; however, identification of thepatient with LOPS can easily be carriedout without this or other expensive equip-ment.

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 (306)suggested that a screening ABI be per-formed in patients over 50 years of ageand be considered in patients under 50years of age who have other PAD risk fac-tors (e.g., smoking, hypertension, hyper-lipidemia, or duration of diabetes �10years). Refer patients with significantsymptoms or a positive ABI for furthervascular assessment and consider exer-cise, medications, and surgical options(306).

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 LOPS,the importance of foot monitoring on adaily basis, the proper care of the foot,including nail and skin care, and the se-lection of appropriate footwear. Patientswith LOPS should be educated on ways tosubstitute other sensory modalities (handpalpation, visual inspection) for surveil-lance of early foot problems. Patients’ un-derstanding 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.

People with neuropathy or evidenceof increased plantar pressure (e.g., ery-thema, warmth, callus, or measured pres-sure) may be adequately managed withwell-fitted walking shoes or athletic shoesthat cushion the feet and redistributepressure. Callus can be debrided with ascalpel 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) mayneed 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.

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.

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. It is appropriate to considerthe unique aspects of care and manage-ment of children and adolescents withtype 1 diabetes. Children with diabetesdiffer from adults in many respects, in-cluding changes in insulin sensitivity re-lated to sexual maturity and physicalgrowth, ability to provide self-care, super-vision in child care and school, andunique neurological vulnerability to hy-poglycemia and DKA. Attention to suchissues as family dynamics, developmentalstages, and physiological differences re-lated to sexual maturity are all essential indeveloping and implementing an optimaldiabetes regimen. Although recommen-dations for children and adolescents areless likely to be based on clinical trial ev-idence, expert opinion and a review ofavailable and relevant experimental dataare summarized in the ADA statement oncare of children and adolescents with type1 diabetes (307).

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 be 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. MNTand psychological support should be pro-vided at diagnosis, and regularly thereaf-ter, by individuals experienced with thenutritional and behavioral needs of thegrowing child and family.

a. Glycemic control

Recommendations● Consider age when setting glycemic

goals in children and adolescents withtype 1 diabetes. (E)

While current standards for diabetesmanagement reflect the need to maintainglucose control as near to normal as safelypossible, special consideration should begiven to the unique risks of hypoglycemiain young children. Glycemic goals mayneed to be modified to take into accountthe fact that most children �6 or 7 yearsof age have a form of “hypoglycemic un-awareness,” including immaturity of anda relative inability to recognize and re-spond to hypoglycemic symptoms, plac-ing them at greater risk for severehypoglycemia and its sequelae. In addi-tion, and unlike the case in adults, youngchildren under the age of 5 years may beat risk for permanent cognitive impair-ment after episodes of severe hypoglyce-mia (308 –310). Furthermore, findingsfrom the DCCT demonstrated that near-normalization of blood glucose levels wasmore difficult to achieve in adolescentsthan adults. Nevertheless, the increasedfrequency of use of basal-bolus regimensand insulin pumps in youth from infancythrough adolescence has been associatedwith more children reaching ADA bloodglucose targets (311,312) in those fami-lies in which both parents and the childwith diabetes participate jointly to per-form the required diabetes-related tasks.Furthermore, recent studies document-ing neurocognitive sequelae of hypergly-cemia in children provide anothercompelling motivation for achieving gly-cemic targets (313,314).

In selecting glycemic goals, the bene-fits on long-term health outcomes ofachieving a lower A1C should be bal-anced against the risks of hypoglycemiaand the developmental burdens of inten-sive regimens in children and youth. Age-specific glycemic and A1C goals arepresented in Table 16.

b. Screening and management ofchronic complications in childrenand adolescents with type 1 diabetes

i. Nephropathy

Recommendations● Annual screening for microalbumin-

uria, with a random spot urine sample



for albumin-to-creatinine (ACR) ra-tio, should be considered once thechild is 10 years of age and has haddiabetes for 5 years. (E)

● Confirmed, persistently elevated ACRon two additional urine specimensfrom different days should be treatedwith an ACE inhibitor, titrated to nor-malization of albumin excretion ifpossible. (E)

ii. Hypertension

Recommendations● Treatment of high-normal blood

pressure (systolic or diastolic bloodpressure 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 isnot reached with 3– 6 months of life-style intervention, pharmacologictreatment should be considered. (E)

● Pharmacologic treatment of hyper-tension (systolic or diastolic bloodpressure consistently above the 95th

percentile for age, sex, and height orconsistently greater than 130/80mmHg, if 95% exceeds that value)should be initiated as soon as the di-agnosis is confirmed. (E)

● ACE inhibitors should be consideredfor the initial treatment of hyperten-sion, following appropriate reproduc-tive counseling due to its potentialteratogenic effects. (E)

● The goal of treatment is a blood pres-sure consistently �130/80 or below the90th percentile for age, sex, and height,whichever is lower. (E)

It is important that blood pressure mea-surements are determined correctly, us-ing the appropriate size cuff, and withthe child seated and relaxed. Hyperten-sion should be confirmed on at leastthree separate days. Normal blood pres-sure levels for age, sex, and height andappropriate methods for determina-tions are available online 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 beforeage 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 con-sidered 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)

Table 16—Plasma blood glucose and A1C goals for type 1 diabetes by age-group

Plasma blood glucose goal range(mg/dl)

A1C (%) RationaleBefore meals Bedtime/overnight

Toddlers and preschoolers(0–6 years)

100–180 110–200 �8.5 • Vulnerability to hypoglycemia• Insulin sensitivity• Unpredictability in dietary intake and

physical activity• A lower goal (�8.0%) is reasonable if

it can be achieved without excessivehypoglycemia

School age (6–12 years) 90–180 100–180 �8 • Vulnerability to hypoglycemia• A lower goal (�7.5%) is reasonable if

it can be achieved without excessivehypoglycemia

Adolescents and young adults(13–19 years)

90–130 90–150 �7.5 • A lower goal (�7.0%) is reasonable ifit 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 modified 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 and to help assess glycemia inthose on basal/bolus regimens.

Position Statement


Treatment● Initial therapy should consist of optimi-

zation of glucose control and MNT us-ing a Step 2 AHA diet aimed at adecrease in the amount of saturated fatin the diet. (E)

● After the age of 10 years, the addition ofa statin in patients who, after MNT andlifestyle changes, have LDL cholesterol�160 mg/dl (4.1 mmol/l), or LDL cho-lesterol �130 mg/dl (3.4 mmol/l) andone or more CVD risk factors, is reason-able. (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 (315–317) and clinical (318)CVD. Although intervention data arelacking, the AHA categorizes childrenwith type 1 diabetes in the highest tier forcardiovascular risk and recommendsboth lifestyle and pharmacologic treat-ment for those with elevated LDL choles-terol levels (319,320). Initial therapyshould be with a Step 2 AHA diet, whichrestricts saturated fat to 7% of total calo-ries 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 (321,322).

Neither long-term safety nor cardio-vascular outcome efficacy of statin ther-apy has been established for children.However, recent studies have shownshort-term safety equivalent to that seenin adults, and efficacy in lowering LDLcholesterol levels, improving endothelialfunction, and causing regression of ca-rotid intimal thickening (323–325). Nostatin is approved for use under the age of10 years, and statin treatment should gen-erally not be used in children with type 1diabetes prior to this age.

iv. Retinopathy

Recommendations● The first ophthalmologic examination

should be obtained once the child is 10years of age and has had diabetes for3–5 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 in dia-betic 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● Children with type 1 diabetes should

be screened for celiac disease by mea-suring tissue transglutaminase oranti-endomysial antibodies, withdocumentation of normal total serumIgA levels, soon after the diagnosis ofdiabetes. (E)

● Testing should be repeated in childrenwith growth failure, failure to gainweight, weight loss, diarrhea, flatu-lence, abdominal pain, or signs of mal-absorption, or in children withfrequent unexplained hypoglycemia ordeterioration in glycemic control. (E)

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

● Children with biopsy-confirmed celiacdisease should be placed on a gluten-free diet and have consultation with adietitian experienced in managing bothdiabetes and celiac disease. (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)(326,327). Symptoms of celiac disease in-clude diarrhea, weight loss or poor weightgain, growth failure, abdominal pain,chronic fatigue, malnutrition due to mal-absorption, other gastrointestinal prob-lems, and unexplained hypoglycemia orerratic blood glucose concentrations.

The advent of routine periodicscreening has led to the diagnosis of celiacdisease in asymptomatic children. Whileseveral studies have documented short-term benefits of gluten restriction ongrowth and bone mineral density inasymptomatic children diagnosed withceliac disease by routine screening, thereis little literature available regarding the

long-term benefit of gluten-free diets inthis population.

vi. Hypothyroidism

Recommendations● Children with type 1 diabetes should be

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

● TSH concentrations should be mea-sured after metabolic control has beenestablished. If normal, they should bere-checked every 1–2 years, or if thepatient develops symptoms of thyroiddysfunction, thyromegaly, or an abnor-mal growth rate. (E)

Auto-immune thyroid disease is the mostcommon autoimmune disorder associ-ated with diabetes, occurring in 17–30%of patients with type 1 diabetes (328). Thepresence of thyroid auto-antibodies ispredictive of thyroid dysfunction, gener-ally hypothyroidism but less commonlyhyperthyroidism (329). Subclinical hy-pothyroidism may be associated withincreased risk of symptomatic hypoglyce-mia (330) and with reduced linear growth(331). Hyperthyroidism alters glucosemetabolism, potentially resulting in dete-rioration of metabolic control.

c. Self-managementNo 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 careBecause a sizable portion of a child’s day isspent in school, close communicationwith and cooperation of school or daycare personnel is essential for optimal di-abetes management, safety, and maximalacademic opportunities. See the ADA po-sition statement on Diabetes Care in theSchool and Day Care Setting (332) for fur-ther discussion.



e. Transition from pediatric to adultcareAs they approach the young adult years,older adolescents are at increasing physi-cal, behavioral, and other risks (333,334).As they leave both their home and theirpediatric diabetes care providers, theseolder teens may become disengaged fromthe health care system, leading to lapses inmedical care and deterioration in glyce-mic control (335). Though scientific evi-dence is limited to date, it is clear thatearly and ongoing attention be given tocomprehensive and coordinated planningfor seamless transition of all youth frompediatric to adult health care (336,337).The National Diabetes Education Pro-gram (NDEP) has materials available tofacilitate this transition process (http://ndep.nih.gov/transitions/).

2. Type 2 diabetesThe incidence of type 2 diabetes in ado-lescents is increasing, especially in ethnicminority populations (21). Distinctionbetween type 1 and type 2 diabetes inchildren can be difficult, since the preva-lence of overweight in children continuesto rise and since autoantigens and ketosismay be present in a substantial number ofpatients with features of type 2 diabetes(including obesity and acanthosis nigri-cans). Such a distinction at the time ofdiagnosis is critical since treatment regi-mens, educational approaches, and di-etary counsel will differ markedlybetween the two diagnoses.

Type 2 diabetes has a significant preva-lence of comorbidities already present at thetime of diagnosis (338). It is recommendedthat blood pressure measurement, a fastinglipid profile, microalbuminuria assessment,and dilated eye examination be performedat the time of diagnosis. Thereafter, screen-ing guidelines and treatment recommen-dations for hypertension, dyslipidemia,microalbuminuria, and retinopathy inyouth with type 2 diabetes are similar tothose for youth with type 1 diabetes. Ad-ditional problems that may need to be ad-dressed include polycystic ovary diseaseand the various comorbidities associatedwith pediatric obesity such as sleep ap-nea, hepatic steatosis, orthopedic compli-cations, and psychosocial concerns. TheADA consensus statement on this subject(23) provides guidance on the preven-tion, screening, and treatment of type 2diabetes and its comorbidities in youngpeople.

3. Monogenic diabetes syndromesMonogenic forms of diabetes (neonataldiabetes or maturity-onset diabetes of theyoung) represent a small fraction of chil-dren with diabetes (�5%), but the readyavailability of commercial genetic testingis now enabling a true genetic diagnosiswith increasing frequency. It is importantto correctly diagnose one of the mono-genic forms of diabetes, as these childrenmay be incorrectly diagnosed with type 1or type 2 diabetes, leading to nonoptimaltreatment regimens and delays in diag-nosing other family members.

The diagnosis of monogenic diabetesshould be considered in the following set-tings: diabetes diagnosed within the first 6months of life; in children with strongfamily history of diabetes but without typ-ical features of type 2 diabetes (nonobese,low-risk ethnic group); in children withmild fasting hyperglycemia (100 –150mg/dl [5.5– 8.5 mmol]), especially ifyoung and nonobese; and in childrenwith diabetes but with negative auto-antibodies without signs of obesity or in-sulin resistance. A recent internationalconsensus document discusses in furtherdetail the diagnosis and management ofchildren with monogenic forms of diabe-tes (339).

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)

● Starting at puberty, preconceptioncounseling should be incorporated inthe routine diabetes clinic visit for allwomen of child-bearing potential. (C)

● 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 prior to concep-tion, since drugs commonly used totreat diabetes and its complicationsmay be contraindicated or not recom-mended in pregnancy, including st-atins, ACE inhibitors, ARBs, and mostnoninsulin therapies. (E)

● Since many pregnancies are un-planned, consider the potential risksand benefits of medications that arecontraindicated in pregnancy in allwomen of childbearing potential, and

counsel women using such medica-tions accordingly. (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 6–8weeks 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. In all five studies, theincidence of major congenital malforma-tions in women who participated in pre-conception care (range 1.0 –1.7% ofinfants) was much lower than the inci-dence in women who did not participate(range 1.4–10.9% of infants) (78). 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 facili-tate preconception diabetes care. Un-fortunately, nearly two-thirds ofpregnancies in women with diabetes areunplanned, leading to a persistent ex-cess of malformations in infants of dia-bet ic mothers . To minimize theoccurrence of these devastating malfor-mations, standard care for all women

Position Statement


with diabetes who have child-bearingpotential, beginning at the onset of pu-berty or at diagnosis, should include 1)education about the risk of malforma-tions associated with unplanned preg-nancies and poor metabolic control;and 2) use of effective contraception atall times, unless the patient has goodmetabolic control and is actively tryingto conceive.

Women contemplating pregnancyneed to be seen frequently by a multi-disciplinary team experienced in themanagement of diabetes before andduring pregnancy. The goals of precon-ception care are to 1) involve and em-power the patient in the management ofher diabetes, 2) achieve the lowest A1Ctest results possible without excessivehypoglycemia, 3) assure effective con-traception until stable and acceptableglycemia is achieved, and 4) identify,evaluate, and treat long-term diabetescomplications such as retinopathy, ne-phropathy, neuropathy, hypertension,and CHD (78).

Among the drugs commonly used inthe treatment of patients with diabetes,a number may be relatively or abso-lutely contraindicated during preg-n a n c y . S t a t i n s a r e c a t e g o r y X(contraindicated for use in pregnancy)and should be discontinued before con-ception, as should ACE inhibitors(340). ARBs are category C (risk cannotbe ruled out) in the first trimester butcategory D (positive evidence of risk) inlater pregnancy and should generally bediscontinued before pregnancy. Sincemany pregnancies are unplanned,health care professionals caring for anywoman of childbearing potential shouldconsider the potential risks and benefitsof medications that are contraindicatedin pregnancy. Women using medica-tions such as statins or ACE inhibitorsneed ongoing family planning counsel-ing. Among the oral antidiabetic agents,metformin and acarbose are classified ascategory B (no evidence of risk in hu-mans) and all others as category C. Po-tential r isks and benefits of oralantidiabetic agents in the preconceptionperiod must be carefully weighed, rec-ognizing that data are insufficient to es-tablish the safety of these agents inpregnancy.

For further discussion of preconcep-tion care, see the ADA’s consensus state-ment on preexisting diabetes andpregnancy (78) and the position state-ment (341) on this subject.

C. Older adults

Recommendations● Older adults who are functional, cogni-

tively intact, and have significant lifeexpectancy should receive diabetes careusing goals developed for youngeradults. (E)

● Glycemic goals for older adults notmeeting 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 time frame 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 preven-tion trials. (E)

● Screening for diabetes 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 (342) have in-fluenced the following discussion andrecommendations. 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 expectedto live long enough to reap the benefits oflong-term intensive diabetes managementand who are active, have good cognitivefunction, and are willing should be pro-vided with the needed education and skillsto 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.However, patients with poorly controlleddiabetes may be subject to acute compli-cations of diabetes, including dehydra-t ion , poor wound hea l ing , andhyperglycemic hyperosmolar coma. Gly-cemic goals at a minimum should avoidthese 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 factorsrather than from tight glycemic controlalone. There is strong evidence from clin-ical trials of the value of treating hyper-tension in the elderly (343,344). There isless evidence for lipid-lowering and aspi-rin therapy, although the benefits of theseinterventions for primary and secondaryprevention are likely to apply to olderadults whose life expectancies equal orexceed the time frames seen in clinicaltrials.

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 York



Heart Association class III and class IV)and if used at all should be used very cau-tiously in those with, or at risk for, milderdegrees of CHF. Sulfonylureas, other in-sulin secretagogues, and insulin can causehypoglycemia. Insulin use requires thatpatients or caregivers have good visualand motor skills and cognitive ability.Drugs should be started at the lowest doseand titrated up gradually until targets arereached or side effects develop.

Screening for diabetes 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.

D. Cystic fibrosis–related diabetesCystic fibrosis–related diabetes (CFRD) isthe most common comorbidity in personswith CF, occurring in about 20% of ado-lescents and 40–50% of adults. The addi-tional diagnosis of diabetes in thispopulation is associated with worse nutri-tional status, more-severe inflammatorylung disease, and greater mortality fromrespiratory failure. For reasons that arenot well understood, women with CFRDare particularly vulnerable to excess mor-bidity and mortality. Insulin insufficiencyrelated to partial fibrotic destruction ofthe islet mass is the primary defect inCFRD. Genetically determined functionof the remaining �-cells and insulin resis-tance associated with infection and in-flammation may also play a role.Encouraging new data suggest that earlydetection and aggressive insulin therapyhave narrowed the gap in mortality be-tween CF patients with and without dia-betes, and have eliminated the sexdifference in mortality.

A consensus conference on CFRDwas co-sponsored in 2009 by the Ameri-can Diabetes Association, the Cystic Fi-brosis Foundation, and the PediatricEndocrine Society. Recommendations forthe clinical management of CFRD can befound in an ADA position statement(344a).

VIII. DIABETES CARE IN SPECIFICSETTINGS

A. Diabetes care in the hospital

Recommendations● All patients with diabetes admitted to

the hospital should have their diabetes

clearly 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: Insulin therapy

should be initiated for treatment ofpersistent hyperglycemia starting at athreshold of no greater than 180mg/dl (10 mmol/l). Once insulintherapy is started, a glucose range of140–180 mg/dl (7.8–10 mmol/l) isrecommended for the majority ofcritically ill patients. (A)

● More stringent goals, such as 110–140 mg/dl (6.1–7.8 mmol/l) may beappropriate for selected patients, aslong as this can be achieved withoutsignificant hypoglycemia. (C)

● Critically ill patients require an intra-venous insulin protocol that hasdemonstrated efficacy and safety inachieving the desired glucose rangewithout increasing risk for severe hy-poglycemia. (E)

● Non–critically ill patients: There isno clear evidence for specific bloodglucose goals. If treated with insulin,the premeal blood glucose targetshould generally be �140 mg/dl (7.8mmol/l) with random blood glucose�180 mg/dl (10.0 mmol/l), providedthese targets can be safely achieved.More stringent targets may be appro-priate in stable patients with previoustight glycemic control. Less stringenttargets may be appropriate in thosewith severe comorbidites. (E)

● Scheduled subcutaneous insulin withbasal, nutritional, and correction com-ponents is the preferred method forachieving and maintaining glucosecontrol in noncritically ill patients. (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 should be initiatedin any patient not known to be diabeticwho receives therapy associated withhigh risk for hyperglycemia, includinghigh-dose glucocorticoid therapy, initi-ation of enteral or parenteral nutrition,or other medications such as octreotideor immunosuppressive medications.(B) If hyperglycemia is documentedand persistent, treatment is necessary.Such patients should be treated to the

same glycemic goals as patients withknown diabetes. (E)

● A hypoglycemia management protocolshould be adopted and implementedby each hospital or hospital system. Aplan for treating hypoglycemia shouldbe established for each patient. Epi-sodes of hypoglycemia in the hospitalshould be documented in the medialrecord and 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)

● 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)

Hyperglycemia in the hospital is exten-sively reviewed in an ADA technical re-view (345). A recent updated consensusstatement by the American Association ofClinical Endocrinologists (AACE) and theADA (346) forms the basis for the discus-sion and guidelines in this section.

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

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

2. Unrecognized diabetes: hyperglycemia(fasting blood glucose �126 mg/dl orrandom blood glucose �200 mg/dl)occurring during hospitalization andconfirmed as diabetes after hospitaliza-tion by standard diagnostic criteria butunrecognized as diabetes by the treat-ing physician during hospitalization.

3. Hospital-related hyperglycemia: hy-perglycemia (fasting blood glucose�126 mg/dl or random blood glucose�200 mg/dl) occurring during thehospitalization that reverts to normalafter hospital discharge.

The management of hyperglycemia in thehospital has often been considered sec-ondary in importance to the conditionthat prompted admission (345). How-ever, a body of literature now supportstargeted glucose control in the hospitalsetting for potential improved clinicaloutcomes. Hyperglycemia in the hospitalmay result from stress, decompensationof type 1 or type 2 or other forms of dia-betes, and/or may be iatrogenic due towithholding of anti-hyperglycemic medi-

Position Statement


cations or administration of hyperglyce-mia -provok ing agen t s such asglucocorticoids or vasopressors.

People with diabetes are more likelyto be hospitalized and to have longerlengths of stay than those without diabe-tes. A recent survey estimated that 22% ofall hospital inpatient days were incurredby people with diabetes and that hospitalinpatient care accounted for half of the$174 billion total U.S. medical expendi-tures for this disease (347). This is due, inpart, to the continued expansion of theworldwide epidemic of type 2 diabetes.While the costs of illness-related stresshyperglycemia are not known, they arelikely to be significant given the poorprognosis of such patients (348–351).

There is substantial observational ev-idence linking hyperglycemia in hospital-ized patients (with or without diabetes) topoor outcomes. Cohort studies as well asa few early randomized controlled trials(RCTs) suggested that intensive treatmentof hyperglycemia improved hospital out-comes (345,350,351). In general, thesestudies were heterogeneous in terms ofpatient population, blood glucose targetsand insulin protocols, provision of nutri-tional support, and the proportion of pa-tients receiving insulin, which limits theability to make meaningful comparisonsamong them. Recent trials in critically illpatients have failed to show a significantimprovement in mortality with intensiveglycemic control (352,353) or have evenshown increased mortality risk (354).Moreover, these recent RCTs have high-lighted the risk of severe hypoglycemiaresulting from such efforts (352–357).

The largest study to date, NICE-SUGAR, a multicenter, multinationalRCT, compared the effect of intensive gly-cemic control (target 81–108 mg/dl,mean blood glucose attained 115 mg/dl)to standard glycemic control (target 144–180 mg/dl, mean blood glucose attained144 mg/dl) on outcomes among 6,104critically ill participants, the majority ofwhom (�95%) required mechanical ven-tilation (354). Ninety-day mortality wassignificantly higher in the intensive versusthe conventional group (78 more deaths;27.5% vs. 24.9%, P � 0.02) in both sur-gical and medical patients. Mortality fromcardiovascular causes was more commonin the intensive group (76 more deaths;41.6% vs. 35.8%; P � 0.02). Severe hy-poglycemia was also more common in theintensively treated group (6.8% vs. 0.5%;P � 0.001). The precise reason for theincreased mortality in the tightly con-

trolled group is unknown. The results ofthis study lie in stark contrast to a famous2001 single-center study that reported a42% relative reduction in intensive-careunit (ICU) mortality in critically ill surgi-cal patients treated to a target blood glu-cose of 80–110 mg/dl (350). Importantly,the control group in NICE-SUGAR hadreasonably good blood glucose manage-ment maintained at a mean glucose of 144mg/dl, only 29 mg/dl above the inten-sively managed patients. Accordingly,this study’s findings do not disprove thenotion that glycemic control in the ICU isimportant. However, they do stronglysuggest that it is not necessary to targetblood glucose values �140 mg/dl, andthat a highly stringent target of �110mg/dl may actually be dangerous.

In a recent meta-analysis of 26 trials(N � 13,567), which included the NICE-SUGAR data, the pooled relative risk (RR)of death with intensive insulin therapywas 0.93 as compared with conventionaltherapy (95% CI 0.83–1.04) (357). Ap-proximately half of these trials reportedhypoglycemia, with a pooled RR of inten-sive therapy of 6.0 (95% CI 4.5–8.0). Thespecific ICU setting influenced the find-ings, with patients in surgical ICUs ap-pearing to benefit from intensive insulintherapy (RR 0.63 [95% CI 0.44–0.91]),while those in other critical care settingsdid not (medical ICU, RR 1.0 [95% CI0.78–1.28]; “mixed” ICU, RR 0.99 [95%CI 0.86–1.12]). It was concluded thatoverall, intensive insulin therapy in-creased the risk of hypoglycemia but pro-vided no overall benefit on mortality inthe critically ill, although a possible mor-tality benefit to patients admitted to thesurgical ICU (RR 0.63 [95% CI 0.44–0.91]) was suggested.

1. Glycemic targets in hospitalizedpatients

Definition of glucose abnormalitiesin the hospital settingHyperglycemia has been defined as anyblood glucose level �140 mg/dl (7.8mmol/l). Levels that are significantly andpersistently above this may require treat-ment in hospitalized patients. In patientswithout a previous diagnosis of diabetes,elevated blood glucose may be due to“stress hyperglycemia,” a condition thatcan be established by a review of priorrecords or measurement of an A1C. A1Cvalues �6.5% suggest that diabetes pre-ceded hospitalization (358). Hypoglyce-mia has been defined as any blood glucose

level �70 mg/dl (3.9 mmol/l). This is thestandard definition in outpatients andcorrelates with the initial threshold for therelease of counterregulatory hormones.Severe hypoglycemia in hospitalized pa-tients has been defined by many as �40mg/dl (2.2 mmol/l), although this is lowerthan the �50 mg/dl (2.8 mmol/l) level atwhich cognitive impairment begins innormal individuals (359). As with hyper-glycemia, hypoglycemia among inpa-tients is also associated with adverseshort- and long-term outcomes. Early rec-ognition and treatment of mild to moder-ate hypoglycemia (40 and 69 mg/dl) (2.2and 3.8 mmol/l) can prevent deteriora-tion to a more severe episode with poten-tial adverse sequelae (346).

Critically ill patientsBased on the weight of the available evi-dence, for the majority of critically ill pa-tients in the ICU setting, insulin infusionshould be used to control hyperglycemia,with a starting threshold of no higher than180 mg/dl (10.0 mmol/l). Once intrave-nous insulin is started, the glucose levelshould be maintained between 140 and180 mg/dl (7.8 and 10.0 mmol/l). Greaterbenefit maybe realized at the lower end ofthis range. Although strong evidence islacking, somewhat lower glucose targetsmay be appropriate in selected patients.However, targets less than 110 mg/dl (6.1mmol/l) are not recommended. Use of in-sulin infusion protocols with demon-strated safety and efficacy, resulting inlow rates of hypoglycemia, are highly rec-ommended (346).

Noncritically ill patientsWith no prospective RCT data to informspecific glycemic targets in noncriticallyill patients, recommendations are basedon clinical experience and judgment. Forthe majority of noncritically ill patientstreated with insulin, premeal glucose tar-gets should generally be �140 mg/dl (7.8mmol/l) with random blood glucose lev-els �180 mg/dl (10.0 mmol/l), as long asthese targets can be safely achieved. Toavoid hypoglycemia, considerationshould be given to reassessing the insulinregimen if blood glucose levels fall below100 mg/dl (5.6 mmol/l). Modification ofthe regimen is required when blood glu-cose values are �70 mg/dl (3.9 mmol/l),unless the event is easily explained byother factors (such as a missed meal, etc.)

Occasional patients with a prior his-tory of successful tight glycemic control inthe outpatient setting who are clinically



stable may be maintained with a glucoserange below the above cut points. Con-versely, higher glucose ranges may be ac-ceptable in terminally ill patients or inpatients with severe comorbidities, aswell as in those in patient-care settingswhere frequent glucose monitoring orclose nursing supervision is not feasible.

Clinical judgment, combined withongoing assessment of the patient’s clini-cal status, including changes in the trajec-tory of glucose measures, the severity ofillness, nutritional status, or concurrentuse of medications that might affect glu-cose levels (e.g., steroids, octreotide)must be incorporated into the day-to-daydecisions regarding insulin dosing (346).

2. Anti-hyperglycemic agents inhospitalized patientsIn the hospital setting, insulin therapy isthe preferred method of glycemic controlin majority of clinical situations (346). Inthe ICU, intravenous infusion is the pre-ferred route of insulin administration.When the patient is transitioned off intra-venous insulin to subcutaneous therapy,precautions should be taken to preventhyperglycemia escape (360,361). Outsideof critical care units, scheduled subcuta-neous insulin which delivers basal, nutri-tional, and correction (supplemental)components is preferred. Prolonged ther-apy with sliding scale insulin (SSI) as thesole regimen is ineffective in the majorityof patients, increases risk of both hypo-glycemia and hyperglycemia, and has re-cently been shown to be associated withadverse outcomes in general surgery pa-tients with type 2 diabetes (362). SSI ispotentially dangerous in type 1 diabetes(346). The reader is referred to severalrecent publications and reviews that de-scribe currently available insulin prepara-tions and protocols and provide guidancein use of insulin therapy in specific clini-cal settings including parenteral nutrition(363), enteral tube feedings, and withhigh-dose glucocorticoid therapy (346).

There are no data on the safety andefficacy of oral agents and injectable non-insulin therapies such as GLP1 analogsand pramlintide in the hospital. They aregenerally considered to have a limited rolein the management of hyperglycemia inconjunction with acute illness. Continua-tion of these agents may be appropriate inselected stable patients who are expectedto consume meals at regular intervals andthey may be initiated or resumed in antic-ipation of discharge once the patient isclinically stable. Specific caution is re-

quired with metformin, due to the possi-bility that a contraindication may developduring the hospitalization, such as renalinsufficiency, unstable hemodynamic sta-tus, or need for an imaging study that re-quires a radio-contrast dye.

3. Preventing hypoglycemiaHypoglycemia, especially in insulin-treated patients, is the leading limitingfactor in the glycemic management oftype 1 and type 2 diabetes (173). In thehospital, multiple additional risk factorsfor hypoglycemia are present. Patientswith or without diabetes may experiencehypoglycemia in the hospital in associa-tion with altered nutritional state, heartfailure, renal or liver disease, malignancy,infection, or sepsis. Additional triggeringevents leading to iatrogenic hypoglycemiainclude sudden reduction of corticoste-roid dose, altered ability of the patient toreport symptoms, reduction of oral in-take, emesis, new NPO status, inappro-priate timing of short- or rapid-actinginsulin in relation to meals, reduction ofrate of administration of intravenous dex-trose, and unexpected interruption of en-teral feedings or parenteral 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 (346).

4. Diabetes care providers in thehospitalInpatient diabetes management may beeffectively championed and/or providedby primary care physicians, endocrinolo-gists, intensivists, or hospitalists. Involve-ment of appropriately trained specialistsor specialty teams may reduce length ofstay, improve glycemic control, and im-prove outcomes (346). In the care of dia-betes, implementation of standardizedorder sets for scheduled and correction-dose insulin may reduce reliance on slid-ing-scale management. As hospitals moveto comply with “meaningful use” regula-tions for electronic health records, asmandated by the Health InformationTechnology Act, efforts should be made toassure that all components of structured in-sulin order sets are incorporated into elec-tronic insulin order sets (364,365).

A team approach is needed to estab-lish hospital pathways. To achieve glyce-mic targets associated with improved

hospital outcomes, hospitals will needmultidisciplinary support to develop in-sulin management protocols that effec-tively and safely enable achievement ofglycemic targets (366).

5. 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 theconditions of hospitalization.

Patients who use CSII pump therapyin the outpatient setting can be candidatesfor diabetes self-management in the hos-pital, provided that they have the mentaland physical capacity to do so (346). Ahospital policy and procedures delineat-ing inpatient guidelines for CSII pumptherapy are advisable. The availability ofhospital personnel with expertise in CSIItherapy is essential. It is important thatnursing personnel document basal ratesand bolus doses taken on a regular basis(at least daily).

6. 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 and/or familymembers receive sufficient informationand training to enable safe care at home.Those newly diagnosed with diabetes orwho are new to insulin and/or blood glu-cose monitoring need to be instructedbefore discharge. Those patients hospital-ized because of a crisis related to diabetesmanagement or poor care at home neededucation to prevent subsequent episodesof hospitalization. An assessment of the

Position Statement


need for a home health referral or referralto an outpatient diabetes education pro-gram should be part of discharge plan-ning for all patients.

7. MNT in the hospitalThe goals of MNT are to optimize glyce-mic control, to provide adequate caloriesto meet metabolic demands, and to createa discharge plan for follow-up care(345,367). ADA does not endorse anysingle meal plan or specified percentagesof macronutrients, and the term “ADAdiet” should no longer be used. Currentnutrition recommendations advise indi-vidualization based on treatment goals,physiologic parameters, and medicationusage. Consistent carbohydrate mealplans are preferred by many hospitalssince they facilitate matching the prandialinsulin dose to the amount of carbohy-drate consumed (368). 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 determinea realistic plan for nutrition therapy(369,370).

8. Bedside blood glucose monitoringPoint-of-care (POC) blood glucose moni-toring performed at the bedside is used toguide insulin dosing. In the patient who isreceiving nutrition, the timing of glucosemonitoring should match carbohydrateexposure. In the patient who is not receiv-ing nutrition, glucose monitoring is per-formed every 4 to 6 h (371,372). Morefrequent blood glucose testing rangingfrom every 30 min to every 2 h is requiredfor patients on intravenous insulin infu-sions.

Safety standards should be estab-lished for blood glucose monitoring, pro-hibiting sharing of fingerstick lancingdevices, lancets, and needles to reduce therisk of transmission of blood borne dis-eases. Shared lancing devices carry essen-tially the same risk as shared syringes andneedles (373).

Accuracy of blood glucose measure-ments using POC meters has limitationsthat must be considered. Although theFDA allows a �20% error for blood glu-cose meters, questions about the appro-priateness of these criteria have beenraised (388). Glucose measures differ sig-nificantly between plasma and whole

blood, terms that are often used inter-changeably and can lead to misinterpre-tation. Most commercially availablecapillary blood glucose meters introducea correction factor of �1.12 to report a“plasma adjusted” value (374).

Significant discrepancies betweencapillary, venous, and arterial plasmasamples have been observed in patientswith low or high hemoglobin concentra-tions, hypoperfusion, and the presence ofinterfering substances particularly mal-tose, as contained in immunoglobulins(375). Analytical variability has been de-scribed with several POC meters (376).Increasingly, newer generation POCblood glucose meters correct for variationin hematocrit and for interfering sub-stances. Any glucose result that does notcorrelate with the patient’s status shouldbe confirmed through conventional labo-ratory sampling of plasma glucose. TheFDA has become increasingly concernedabout the use of POC blood glucosemeters in the hospital and is presently re-viewing matters related to their use.

9. Discharge planningTransition from the acute care setting is ahigh-risk time for all patients, not justthose with diabetes or new hyperglyce-mia. Although there is an extensive liter-ature concerning safe transition withinand from the hospital, little of it is specificto diabetes (377). It is important to re-member that diabetes discharge planningis not a separate entity, but part of anoverall discharge plan. As such, dischargeplanning begins at admission to the hos-pital and is updated as projected patientneeds change.

Inpatients may be discharged to var-ied settings, including home (with orwithout visiting nurse services), assistedliving, rehabilitation, or skilled nursingfacilities. The latter two sites are generallystaffed by health professionals; thereforediabetes discharge planning will be lim-ited to communication of medication anddiet orders. For the patient who is dis-charged to assisted living or to home, theoptimal program will need to consider thetype and severity of diabetes, the effects ofthe patient’s illness on blood glucose lev-els, and the capacities and desires of thepatient. Smooth transition to outpatientcare should be ensured. The Agency forHealthcare Research and Quality recom-mends that at a minimum, dischargeplans include:

● Medication reconciliation: The pa-tient’s medications must be cross-checked to ensure that no chronicmedications were stopped and to en-sure the safety of new prescriptions.Whenever possible, prescriptions fornew or changed medication should befilled and reviewed with the patient andfamily at or before discharge

● Structured discharge communication:Information on medication changes,pending tests and studies, and fol-low-up needs must be accurately andpromptly communicated to outpatientphysicians, as soon as possible after dis-charge.

Ideally the inpatient care providers orcase managers/discharge planners willschedule follow-up visit(s) with the ap-propriate professionals, including pri-mary care provider, endocrinologist, anddiabetes educator (378).

An outpatient follow-up visit with theprimary care provider, endocrinologist,or diabetes educator within 1 month ofdischarge is advised for all patients havinghyperglycemia in the hospital. Clear com-munication with outpatient providers ei-ther directly or via hospital dischargesummaries facilitates safe transitions tooutpatient care. Providing information re-garding the cause or the plan for deter-mining the cause of hyperglycemia,related complications and comorbidities,and recommended treatments can assistoutpatient providers as they assume on-going care.

It is important that patients be pro-vided with appropriate durable medicalequipment, medication, supplies, andprescriptions at the time of discharge inorder to avoid a potentially dangerous hi-atus in care. These supplies/prescriptionsshould include:

● Insulin (vials or pens) (if needed)● Syringes or pen needles (if needed)● Oral medications (if needed)● Blood glucose meter and strips● Lancets and lancing device● Urine ketone strips (type 1)● Glucagon emergency kit (insulin-

treated)● Medical alert application/charm

IX. STRATEGIES FORIMPROVING DIABETESCARE — There has been steady im-provement in the proportion of diabeticpatients achieving recommended levels ofA1C, blood pressure, and LDL cholesterol



in the last 10 years, both in primary caresettings and in endocrinology practices.Mean A1C nationally has declined from7.82% in 1999–2000 to 7.18% in 2004based on National Health and NutritionExamination Survey (NHANES) data(379). This has been accompanied by im-provements in lipids and blood pressurecontrol and led to substantial reductionsin end-stage microvascular complicationsin those with diabetes (380). Neverthe-less, in some studies only 57.1% of adultswith diagnosed diabetes achieved an A1Cof �7%, only 45.5% had a blood pressure�130/80 mmHg, and just 46.5% had atotal cholesterol �200 mg/dl, with only12.2% of people with diabetes achievingall three treatment goals (381). Moreover,there is persistent variation in quality ofdiabetes care across providers and acrosspractice settings even after adjusting forpatient factors that indicates the potentialfor substantial further improvements indiabetes care.

While numerous interventions to im-prove adherence to the recommendedstandards have been implemented, a ma-jor contributor to suboptimal care is a de-livery system that too often is fragmented,lacks clinical information capabilities, of-ten duplicates services, and is poorly de-signed for the delivery of chronic care.The Chronic Care Model (CCM) includessix core elements for the provision of op-timal care of patients with chronic dis-ease: 1) delivery system design (movingfrom a reactive to a proactive care deliverysystem, where planned visits are coordi-nated through a team-based approach; 2)self-management support; 3) decisionsupport (basing care on consistent, effec-tive care guidelines); 4) clinical informa-tion systems (using registries that canprovide patient-specific and population-based support to the care team); 5)community resources and policies (iden-tifying or developing resources to supporthealthy lifestyles); and 6) health systems(to create a quality-oriented culture). Al-terations in reimbursement that rewardthe provision of quality care, as defined bythe attainment of evidence-based qualitymeasures, will also be required to achievedesired outcome goals. Redefinition of theroles of the clinic staff and promoting self-management on the part of the patient arefundamental to the successful implemen-tation of the CCM (382). Collaborative,multidisciplinary teams are best suited toprovide such care for people with chronicconditions like diabetes and to facilitate

patients’ performance of appropriate self-management.

A rapidly evolving literature suggeststhat there are three major strategies tosuccessfully improve the quality of diabe-tes care delivered by a team of providers.NDEP maintains an online resource(www.betterdiabetescare.nih.gov) to helphealth care professionals design and im-plement more effective health care deliv-ery systems for those with diabetes.

Three specific objectives, with refer-ences to literature that outlines practicalstrategies to achieve each, are outlined be-low.

Objective 1Provider and team behavior change: Fa-cilitate timely and appropriate intensifica-tion of lifestyle and/or pharmaceuticaltherapy of patients who have not achievedbeneficial levels of blood pressure, lipid,or glucose control.

● Clinical information systems includingregistries that can prospectively iden-tify and track those requiring assess-ments and/or treatment modificationsby the team.

● Electronic medical record-based clini-cal decision support at the point of care,both personalize and standardize careand can be used by multiple providers(383).

● Use of checklists and/or flow sheets thatmirror guidelines.

● Detailed treatment algorithms enablingmultiple team members to “treat to tar-get” and appropriately intensify ther-apy.

● Availability of care or disease manage-ment services (384) by nurses, pharma-cists, and other providers usingdetailed algorithms often catalyzing re-duction in A1C, blood pressure, andLDL cholesterol (385,386).

Objective 2Patient behavior change: Implement asystematic approach to support patients’behavior change efforts as needed includ-ing 1) healthy lifestyle (physical activity,healthy eating, nonuse of tobacco, weightmanagement, effective coping, medica-tion taking and management); 2) preven-tion of diabetes complications (screeningfor eye, foot, and renal complications; im-munizations); and 3) achievement of ap-propriate blood pressure, lipid, andglucose goals.

● Delivery of high-quality DSME, whichhas been shown to improve patient self-management, satisfaction, and glucosecontrol (115,387).

● Delivery of ongoing diabetes self-management support (DSMS) to ensurethat gains achieved during DSME aresustained (128–129). National DSMEstandards call for an integrated ap-proach that includes clinical contentand skills, behavioral strategies (goal-setting, problem solving), and address-ing emotional concerns in each neededcurriculum content area. Provision ofcontinuing education and support(DSMS) improves maintenance of gainsregardless of the educational methodol-ogy (89).

● Provision of automated reminders viamultiple communication channels tovarious subgroups of diabetic patients(96).

Objective 3Change the system of care: Research onthe comprehensive CCM suggests addi-tional strategies to improve diabetes care,including the following:

● Basing care on consistent, evidence-based care guidelines

● Redefining and expanding the roles ofthe clinic staff (382)

● Collaborative, multidisciplinary teamsto provide high-quality care and sup-port patients ’ appropriate sel f-management

● Audit and feedback of process and out-come data to providers to encouragepopulation-based care improvementstrategies

● Care management, one of the most ef-fective diabetes quality improvementstrategies to improve glycemic control(384).

● Identifying and/or developing commu-nity resources and public policy thatsupport healthy lifestyles

● Alterations in reimbursement that re-ward the provision of appropriate andhigh-quality care and accommodate theneed to personalize care goals, provid-ing additional incentives to improve di-abetes care (382,388–392)

The most successful practices have an in-stitutional priority for quality of care, ex-panding the role of teams and staff,redesigning their delivery system, activat-ing and educating their patients, and us-ing electronic health record tools(393,394). Recent initiatives such as the

Position Statement


Patient Centered Medical Home showpromise in improving outcomes throughcoordinated primary care and offer newopportunities for team-based chronic dis-ease care (395).

It is clear that optimal diabetes man-agement requires an organized, system-atic approach and involvement of acoordinated team of dedicated health careprofessionals working in an environmentwhere patient-centered high-quality careis a priority.

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Position Statement


Ada2011

Education

Transcript of Ada2011