ada 2012

Introduction

The American Diabetes Association(ADA) has been actively involved inthe development and dissemination

of diabetes care standards, guidelines, andrelated documents for many years. Thesestatements are published in one or moreof the Association’s professional journals.This supplement contains the latest up-date of ADA’s major position statement,“Standards of Medical Care in Diabetes,”which contains all of the Association’s keyrecommendations. In addition, containedherein are selected position statements oncertain topics not adequately covered inthe “Standards.” ADA hopes that this is aconvenient and important resource for allhealth care professionals who care forpeople with diabetes.

ADA Clinical Practice Recommenda-tions consist of position statements thatrepresent official ADA opinion as denotedby formal review and approval by theProfessional Practice Committee and theExecutive Committee of the Board ofDirectors. Consensus reports and system-atic reviews are not official ADA recom-mendations; however, they are producedunder the auspices of the Association byinvited experts. These publications maybe used by the Professional Practice Com-mittee as source documents to update the“Standards.”

ADA has adopted the following def-initions for its clinically related reports.

ADA position statement. An officialpoint of view or belief of the ADA.Position statements are issued on scien-tific or medical issues related to diabetes.They may be authored or unauthored andare published in ADA journals and otherscientific/medical publications as appro-priate. Position statements must be re-viewed and approved by the ProfessionalPractice Committee and, subsequently,by the Executive Committee of the Boardof Directors. ADA position statements aretypically based on a systematic reviewor other review of published literature.

They are reviewed on an annual basis andupdated as needed. A list of recent posi-tion statements is included on p. e114 ofthis supplement.

Systematic review. A balanced reviewand analysis of the literature on a scien-tific or medical topic related to diabetes.Effective January 2010, technical reviewsare replaced with systematic reviews, forwhich a priori search and inclusion/exclusion criteria are developed and pub-lished. The systematic review provides ascientific rationale for a position state-ment and undergoes critical peer reviewbefore submission to the ProfessionalPractice Committee for approval. A listof past technical reviews is included onpage e110 of this supplement.

Consensus report. A comprehensive ex-amination by a panel of experts (i.e., con-sensus panel) of a scientific or medicalissue related to diabetes. Effective January2010, consensus statements were re-named consensus reports. The categorynow also includes task force, workgroup,and expert committee reports. Consensusreports do not have the Association’sname included in the title or subtitle andinclude a disclaimer in the introductionstating that any recommendations are notADA position. A consensus report is typi-cally developed immediately following aconsensus conference at which presenta-tions are made on the issue under review.The statement represents the panel’s col-lective analysis, evaluation, and opinion atthat point in time based in part on theconference proceedings. The need for aconsensus report arises when clinicians orscientists desire guidance on a subject forwhich the evidence is contradictory or in-complete. Once written by the panel, aconsensus report is not subject to subse-quent review or approval and does notrepresent official Association opinion. Alist of recent consensus reports is includedon p. e112 of this supplement.

Professional Practice Committee. TheAssociation ’s Professional PracticeCommittee is responsible for reviewingADA systematic reviews and positionstatements, as well as for overseeingrevisions of the latter as needed. Ap-pointment to the Professional PracticeCommittee is based on excellence inclinical practice and/or research. Thecommittee comprises physicians, diabe-tes educators, registered dietitians, andothers who have expertise in a range ofareas, including adult and pediatricendocrinology, epidemiology, and pub-lic health, lipid research, hypertension,and preconception and pregnancy care.All members of the Professional PracticeCommittee are required to disclose po-tential conflicts of interest (listed onpage S109).

Grading of scientific evidence. Therehas been considerable evolution in theevaluation of scientific evidence and inthe development of evidence-basedguidelines since the ADA first beganpublishing practice guidelines. Accord-ingly, we developed a classification sys-tem to grade the quality of scientificevidence supporting ADA recommenda-tions for all new and revised ADA positionstatements.

Recommendations are assigned rat-ings of A, B, or C, depending on thequality of evidence (Table 1). Expertopinion (E) is a separate category forrecommendations in which there is asyet no evidence from clinical trials, inwhich clinical trials may be impractical,or in which there is conflicting evidence.Recommendations with an “A” ratingare based on large well-designed clinicaltrials or well-done meta-analyses. Gen-erally, these recommendations have thebest chance of improving outcomeswhen applied to the population towhich they are appropriate. Recommen-dations with lower levels of evidencemay be equally important but are notas well supported. The level of evidencesupporting a given recommendation isnoted either as a heading for a group ofrecommendations or in parenthesesafter a given recommendation.

Of course, evidence is only one compo-nent of clinical decision-making. Clinicians

c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c

DOI: 10.2337/dc12-s001.© 2012 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 thework is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.

care.diabetesjournals.org DIABETES CARE, VOLUME 35, SUPPLEMENT 1, JANUARY 2012 S1

www.rinconmedico.org

care for patients, not populations;guidelines must always be interpretedwith the needs of the individual patientin mind. Individual circumstances,such as comorbid and coexisting dis-eases, age, education, disability, and,above all, patients’ values and prefer-ences, must also be considered and maylead to different treatment targets andstrategies. Also, conventional evidencehierarchies, such as the one adapted bythe ADA, may miss some nuances thatare important in diabetes care. Forexample, while there is excellent evi-dence from clinical trials supporting theimportance of achieving glycemic con-trol, the optimal way to achieve thisresult is less clear. It is difficult to assesseach component of such a complexintervention.

ADA will continue to improve andupdate the Clinical Practice Recommen-dations to ensure that clinicians, healthplans, and policymakers can continue torely on them as the most authoritative andcurrent guidelines for diabetes care. OurClinical Practice Recommendations arealso available on the Association’s websiteat www.diabetes.org/diabetescare.

Table 1dADA evidence-grading system for clinical practice recommendations

Level ofevidence Description

A Clear evidence from well-conducted, generalizable, randomized controlled trialsĆ that are adequately powered, including:

c Evidence from a well-conducted multicenter trialc Evidence from a meta-analysis that incorporated quality ratings in theĆ analysis

Compelling nonexperimental evidence, i.e., the “all or none” rule developed byĆ the Centre for Evidence-Based Medicine at OxfordSupportive evidence from well-conducted randomized controlled trials that areĆ adequately powered, including:

c Evidence from a well-conducted trial at one or more institutionsc Evidence from a meta-analysis that incorporated quality ratings in theĆ analysis

B Supportive evidence from well-conducted cohort studies, including:c Evidence from a well-conducted prospective cohort study or registryc Evidence from a well-conducted meta-analysis of cohort studies

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

c Evidence from randomized clinical trials with one ormoremajor or Ćthree ormoreĆ minor methodological flaws that could invalidate the resultsc Evidence from observational studies with high potential for bias (such as caseĆ series with comparison to historical controls)c Evidence from case series or case reports

Conflicting evidence with the weight of evidence supporting the recommendationE Expert consensus or clinical experience

S2 DIABETES CARE, VOLUME 35, SUPPLEMENT 1, JANUARY 2012 care.diabetesjournals.org

Introduction

Summary of Revisions for the 2012Clinical Practice Recommendations

Additions to the Standardsof Medical Care inDiabetesd2012c A section on driving and diabetes hasbeen added.

c A section and table on common co-morbidities of diabetes has been added.

c A table listing properties of noninsulintherapies for hyperglycemia in type 2diabetes has been added.

Revisions to the Standardsof Medical Care inDiabetesd2012In addition to many small changes relatedto new evidence since the prior year, and

to clarify recommendations, the follow-ing sections have undergone majorchanges:

c The Introduction was revised to moreclearly describe processes for system-atic evidence review, to link to the ev-idence table for changes since 2011,and to link to opportunities for publiccomment on the Standards of MedicalCare in Diabetesd2012.

c Section V.D.2. Therapy for Type 2 Di-abetes was revised to include more spe-cific recommendations for starting andadvancing pharmacotherapy for hyper-glycemia.

c Section X. Strategies for ImprovingDiabetes Care was revised to reflectgrowing evidence for the effectivenessof restructuring systems of chronic caredelivery.

Revised Position Statementc A revised position statement, “DiabetesManagement at Camps for Childrenwith Diabetes,” has been added.

New Position Statementc A new position statement, “Driving andDiabetes,” has been added.


DOI: 10.2337/dc12-s003© 2012 by the American Diabetes Association. Readers may use this article as long as the work is properly



S U M M A R Y O F R E V I S I O N S

Executive Summary: Standards ofMedical Care in Diabetesd2012

Current criteria for thediagnosis of diabetesc A1C $6.5%. The test should be per-formed in a laboratory using a methodthat is National Glycohemoglobin Stan-dardization Program (NGSP)-certifiedand standardized to the Diabetes Con-trol and Complications Trial (DCCT)assay; or

c fasting plasma glucose (FPG) $126mg/dL (7.0 mmol/l). Fasting is de-fined as no caloric intake for at least8 h; or

c 2-h plasma glucose$200 mg/dL (11.1mmol/l) during an oral glucose toler-ance test (OGTT). The test should beperformed as described by the WorldHealth Organization, using a glucoseload containing the equivalent of 75 ganhydrous glucose dissolved in wa-ter; or

c in a patient with classic symptoms ofhyperglycemia or hyperglycemic crisis,a random plasma glucose $200 mg/dL(11.1 mmol/l);

c in the absence of unequivocal hypergly-cemia, the result should be confirmed byrepeat testing.

Testing for diabetes inasymptomatic patientsc Testing to detect type 2 diabetes and toassess 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 (see Table 4 of the “Standardsof Medical Care in Diabetesd2012”). Inthose without these risk factors, testingshould begin at age 45 years. (B)

c If tests are normal, repeat testing atleast at 3-year intervals is reasonable.(E)

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

c In those identified with increased riskfor future diabetes, identify and, if ap-propriate, treat other cardiovascular dis-ease (CVD) risk factors. (B)

Detection and diagnosis ofgestational diabetesmellitus (GDM)c Screen for undiagnosed type 2 diabetesat the first prenatal visit in those withrisk factors, using standard diagnosticcriteria. (B)

c In pregnant women not previouslyknown to have diabetes, screen forGDM at 24-28 weeks gestation, using a75-g 2-h OGTT and the diagnosticcutpoints in Table 6 of the “Standardsof Medical Care in Diabetesd2012”.(B)

c Screenwomenwith GDM for persistentdiabetes at 6–12 weeks postpartum,using a test other than A1C. (E)

c Women with a history of GDM shouldhave lifelong screening for the devel-opment of diabetes or prediabetes atleast every 3 years. (B)

c Women with a history of GDM foundto have prediabetes should receivelifestyle interventions or metformin toprevent diabetes. (A)

Prevention/delay of type 2diabetesc Patients with IGT (A), IFG (E), or anA1C of 5.7–6.4% (E) should be re-ferred to an effective ongoing sup-port program targeting weight loss of7% of body weight and increasingphysical activity to at least 150 minper week of moderate activity such aswalking.

c Follow-up counseling appears to beimportant for success. (B)

c Based on the cost-effectiveness of dia-betes prevention, such programs shouldbe covered by third-party payers. (B)

c Metformin therapy for prevention oftype 2 diabetes may be considered in

thosewith IGT (A), IFG (E), or anA1Cof5.7–6.4% (E), especially for those withBMI.35 kg/m2, those aged,60 years,and those with prior GDM. (A)

c At least annual monitoring for the de-velopment of diabetes in those withprediabetes is suggested. (E)

Glucose monitoringc Self-monitoring of blood glucose (SMBG)should be carried out three or moretimes daily for patients using multipleinsulin injections or insulin pump ther-apy. (B)

c For patients using less frequent insulininjections, noninsulin therapies, or med-ical nutrition therapy (MNT) alone,SMBG may be useful as a guide to man-agement. (E)

c To achieve postprandial glucose tar-gets, postprandial SMBG may be ap-propriate. (E)

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

c 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)

c Although the evidence for A1C-loweringis less strong in children, teens, andyounger adults, CGM may be helpful inthese groups. Success correlates withadherence to ongoing use of the de-vice. (C)

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

A1Cc Perform the A1C test at least two timesa year in patients who are meeting treat-ment goals (and who have stable glyce-mic control). (E)

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

c Use of point-of-care testing for A1Cprovides the opportunity formore timelytreatment changes. (E)





E X E C U T I V E S U M M A R Y

Glycemic goals in adultsc Lowering A1C to below or around 7%has been shown to reduce microvascularcomplications of diabetes, and if im-plemented soon after the diagnosis ofdiabetes is associated with long-termreduction in macrovascular disease.Therefore, a reasonable A1C goal formany nonpregnant adults is ,7%. (B)

c Providers might reasonably suggest morestringent A1C goals (such as,6.5%) forselected individual patients, if this canbe achieved without significant hypo-glycemia or other adverse effects oftreatment. Appropriate patients mightinclude those with short duration ofdiabetes, long life expectancy, and nosignificant CVD. (C)

c Less stringent A1C goals (such as,8%) may be appropriate for patientswith a history of severe hypoglycemia,limited life expectancy, advanced micro-vascular or macrovascular complications,and extensive comorbid conditions andfor those with longstanding diabetesin whom the general goal is difficult toattain despite diabetes self-managementeducation, appropriate glucose moni-toring, and effective doses of multipleglucose-lowering agents including in-sulin. (B)

Therapy for type 2 diabetesc At the time of type 2 diabetes diagnosis,initiate metformin therapy along withlifestyle interventions, unless metforminis contraindicated. (A)

c In newly diagnosed type 2 diabeticpatients with markedly symptomaticand/or elevated blood glucose levels orA1C, consider insulin therapy, with orwithout additional agents, from the out-set. (E)

c If noninsulin monotherapy at maxi-mal tolerated dose does not achieveor maintain the A1C target over 3–6months, add a secondoral agent, aGLP-1receptor agonist, or insulin. (E)

Medical nutrition therapy(MNT)General Recommendationsc Individuals who have prediabetes ordiabetes should receive individualizedMNT as needed to achieve treatmentgoals, preferably provided by a regis-tered dietitian familiar with the com-ponents of diabetes MNT. (A)

c Because MNT can result in cost-savingsand improvedoutcomes (B),MNTshouldbe adequately covered by insuranceand other payers. (E)

Recommendations for energybalance, overweight, and obesityc Weight loss is recommended for alloverweight or obese individuals whohave or are at risk for diabetes. (A)

c For weight loss, either low-carbohydrate,low-fat calorie-restricted, or Mediterra-nean diets may be effective in the shortterm (up to 2 years). (A)

c For patients on low-carbohydrate di-ets, monitor lipid profiles, renal func-tion, and protein intake (in those withnephropathy) and adjust hypoglyce-mic therapy as needed. (E)

c Physical activity and behavior modi-fication are important components ofweight loss programs and are most help-ful in maintenance of weight loss. (B)

Recommendations for primaryprevention of diabetesc Among individuals at high risk for de-veloping type 2 diabetes, structured pro-grams that emphasize lifestyle changesthat include moderate weight loss (7%body weight) and regular physical ac-tivity (150 min/week), with dietarystrategies that include reduced caloriesand reduced intake of dietary fat, canreduce the risk for developing diabetesand are therefore recommended. (A)

c Individuals at risk for type 2 diabetesshould be encouraged to achieve the U.S.Department of Agriculture (USDA) rec-ommendation for dietaryfiber (14 gfiber/1,000 kcal) and foods containing wholegrains (one-half of grain intake). (B)

c Individuals at risk for type 2 diabetesshould be encouraged to limit theirintake of sugar-sweetened beverages. (B)

Recommendations for managementof diabetesMacronutrients in diabetes managementc The mix of carbohydrate, protein, andfat may be adjusted to meet the meta-bolic goals and individual preferencesof the person with diabetes. (C)

c Monitoring carbohydrate intake, whetherby carbohydrate counting, choices, orexperience-based estimation, remains akey strategy in achieving glycemic con-trol. (B)

c Saturated fat intake should be ,7% oftotal calories. (B)

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

Other nutrition recommendations.c If adults with diabetes choose to usealcohol, they should limit intake to a

moderate amount (one drink per day orless for adult women and two drinks perday or less for adult men) and shouldtake extra precautions to prevent hypo-glycemia. (E)

c Routine supplementation with anti-oxidants, 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)

c It is recommended that individualizedmeal planning include optimization offood choices to meet recommendeddaily allowance (RDA)/dietary referenceintake (DRI) for all micronutrients. (E)

Diabetes self-managementeducation (DSME)c People with diabetes should receiveDSME according to national standardsand diabetes self-management supportat the time their diabetes is diagnosedand as needed thereafter. (B)

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

c DSME should address psychosocial is-sues, since emotional wellbeing is associ-ated with positive diabetes outcomes. (C)

c Because DSME can result in cost-savingsand improved outcomes (B), DSMEshould be adequately reimbursed bythird-party payers. (E)

Physical activityc People with diabetes should be advisedto perform at least 150 min/week ofmoderate-intensity aerobic physical ac-tivity (50–70% of maximum heart rate),spread over at least 3 days per week withno more than 2 consecutive days with-out exercise. (A)

c In the absence of contraindications,people with type 2 diabetes should beencouraged to perform resistance train-ing at least twice per week. (A)

Psychosocial assessmentand carec It is reasonable to include assessmentof the patient’s psychological and so-cial situation as an ongoing part of themedical management of diabetes. (E)

c Psychosocial screening and follow-upmay include, but is not limited to, atti-tudes about the illness, expectations formedical management and outcomes,affect/mood, general and diabetes-relatedquality of life, resources (financial, so-cial, and emotional), and psychiatrichistory. (E)


Executive Summary

c Consider screening for psychosocial prob-lems such as depression and diabetes-related distress, anxiety, eating disorders,and cognitive impairment when self-management is poor. (C)

Hypoglycemiac Glucose (15–20 g) is the preferred treat-ment for the conscious individual withhypoglycemia, although any form of car-bohydrate that contains glucose may beused. If SMBG 15 min after treatmentshows continued hypoglycemia, the treat-ment should be repeated. Once SMBGglucose returns to normal, the individualshould consume a meal or snack to pre-vent recurrence of hypoglycemia. (E)

c 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)

c 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 hy-poglycemia unawareness and reducerisk of future episodes. (B)

Bariatric surgeryc Bariatric surgery may be considered foradults with BMI.35 kg/m2 and type 2diabetes, especially if the diabetes orassociated comorbidities are difficult tocontrol with lifestyle and pharmaco-logic therapy. (B)

c Patients with type 2 diabetes who haveundergone bariatric surgery need life-long lifestyle support and medical mon-itoring. (B)

c Although small trials have shown glyce-mic benefit of bariatric surgery in patientswith type 2 diabetes and BMI of 30–35 kg/m2, there is currently insufficientevidence to generally recommend sur-gery in patients with BMI ,35 kg/m2

outside of a research protocol. (E)c The long-term benefits, cost-effectiveness,and risks of bariatric surgery in indi-viduals with type 2 diabetes should bestudied inwell-designed controlled trialswith optimal medical and lifestyle ther-apy as the comparator. (E)

Immunizationc Annually provide an influenza vaccineto all diabetic patients $6 months ofage. (C)

c Administer pneumococcal polysaccharidevaccine to all diabetic patients $2 yearsof age. A one-time revaccination is rec-ommended for individuals.64 years ofage previously immunized when theywere ,65 years of age if the vaccinewas administered.5 years ago. Otherindications for repeat vaccination in-clude nephrotic syndrome, chronic renaldisease, and other immunocompro-mised states, such as after transplan-tation. (C)

c Administer hepatitis B vaccination toadults with diabetes as per Centers forDisease Control and Prevention (CDC)recommendations. (C)

Hypertension/bloodpressure controlScreening and diagnosisc Blood pressure should be measured atevery routinediabetes visit. Patients foundto have systolic blood pressure $130mmHg or diastolic blood pressure $80mmHg should have blood pressureconfirmed on a separate day. Repeatsystolic blood pressure$130 mmHg ordiastolic blood pressure $80 mmHgconfirms a diagnosis of hypertension. (C)

Goalsc A goal systolic blood pressure ,130mmHg is appropriate for most patientswith diabetes. (C)

c Based on patient characteristics andresponse to therapy, higher or lowersystolic blood pressure targets may beappropriate. (B)

c Patients with diabetes should be trea-ted to a diastolic blood pressure ,80mmHg. (B)

Treatmentc Patients with a systolic blood pressureof 130–139 mmHg or a diastolic bloodpressure of 80–89 mmHgmay be givenlifestyle therapy alone for a maximumof 3 months and then, if targets are notachieved, may be treated with the ad-dition of pharmacological agents. (E)

c Patients with more severe hypertension(systolic blood pressure $140 or di-astolic blood pressure $90 mmHg) atdiagnosis or follow-up should receivepharmacologic therapy in addition tolifestyle therapy. (A)

c Lifestyle therapy for hypertension con-sists ofweight loss, if overweight; DASH-style dietary pattern, including reducingsodium and increasing potassium in-take; moderation of alcohol intake; andincreased physical activity. (B)

c Patients with diabetes and hypertensionshould be treated with a pharmacologictherapy regimen that includes either anACE inhibitor or an ARB). If one class isnot tolerated, the other should besubstituted. (C)

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

c Administer one or more antihyperten-sive medications at bedtime. (A)

c If ACE inhibitors, ARBs, or diuretics areused, kidney function and serum potas-sium levels should be monitored. (E)

c In pregnant patients with diabetes andchronic hypertension, blood pressure tar-get goals of 110–129/65–79 mmHg aresuggested in the interest of long-termmaternal health andminimizing impairedfetal growth. ACE inhibitors and ARBsare contraindicatedduringpregnancy. (E)

Dyslipidemia/lipidmanagementScreeningc In most adult patients, measure fastinglipid profile at least annually. In adultswith low-risk lipid values (LDL choles-terol,100mg/dL,HDL cholesterol.50mg/dL, and triglycerides ,150 mg/dL),lipid assessments may be repeated every2 years. (E)

Treatment recommendationsand goalsc Lifestyle modification focusing on thereduction of saturated fat, trans fat, andcholesterol intake; increase of n-3 fattyacids, viscous fiber and plant stanols/sterols; weight loss (if indicated); andincreased physical activity should berecommended to improve the lipidprofile in patients with diabetes. (A)

c Statin therapy should be added to life-style therapy, regardless of baseline lipidlevels, for diabetic patients:

c with overt CVD. (A)c without CVD who are over the age of40 years and have one or more otherCVD risk factors. (A)

c For lower-risk patients than the above(e.g., without overt CVD and under theage of 40 years), statin therapy shouldbe considered in addition to lifestyletherapy if LDL cholesterol remains.100mg/dL or in those with multiple CVDrisk factors. (E)

c In individuals without overt CVD, theprimary goal is LDL cholesterol ,100mg/dL (2.6 mmol/l). (A)


Executive Summary

c In individuals with overt CVD, a lowerLDL cholesterol goal of ,70 mg/dL(1.8 mmol/l), using a high dose of astatin, is an option. (B)

c If drug-treated patients do not reachthe above targets on maximal toleratedstatin therapy, a reduction in LDL cho-lesterol of;30–40% from baseline is analternative therapeutic goal. (A)

c Triglycerides levels ,150 mg/dL (1.7mmol/l) and HDL cholesterol .40 mg/dL (1.0 mmol/l) in men and.50mg/dL(1.3 mmol/l) in women, are desirable.However, LDL cholesterol–targeted statintherapy remains thepreferred strategy. (C)

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)

c Statin therapy is contraindicated inpregnancy. (B)

Antiplatelet agentsc 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)

c Aspirin should not be recommendedfor CVD prevention for adults withdiabetes at low CVD risk (10-year CVDrisk ,5%, such as in men ,50 yearsand women ,60 years of age with nomajor additional CVD risk factors),since the potential adverse effects frombleeding likely offset the potentialbenefits. (C)

c In patients in these age-groups withmultiple other risk factors (e.g., 10-yearrisk 5–10%), clinical judgment is re-quired. (E)

c Use aspirin therapy (75–162mg/day) as asecondary prevention strategy in thosewith diabetes with a history of CVD. (A)

c For patients with CVD and documentedaspirin allergy, clopidogrel (75 mg/day)should be used. (B)

c 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)

Smoking cessationc Advise all patients not to smoke. (A)

c Include smoking cessation counsel-ing and other forms of treatment asa routine component of diabetes care.(B)

Coronary heart disease (CHD)screening and treatmentScreeningc In asymptomatic patients, routine screen-ing for coronary artery disease (CAD) isnot recommended, as it does not im-prove outcomes as long as CVD riskfactors are treated. (A)

Treatmentc In patients with known CVD, considerACE inhibitor therapy (C) and use as-pirin and statin therapy (A) (if notcontraindicated) to reduce the risk ofcardiovascular events. In patients with aprior myocardial infarction, b-blockersshould be continued for at least 2 yearsafter the event. (B)

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

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

c Metformin may be used in patients withstable congestive heart failure (CHF) ifrenal function is normal. It should beavoided in unstable or hospitalized pa-tients with CHF. (C)

Nephropathy screeningand treatmentGeneral recommendationsc To reduce the risk or slow the progres-sion of nephropathy, optimize glucosecontrol. (A)

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

Screeningc Perform an annual test to assess urinealbumin excretion (UAE) in type 1 di-abetic patients with diabetes durationof $5 years and in all type 2 diabeticpatients starting at diagnosis. (B)

c Measure serum creatinine at least annu-ally in all adults with diabetes regardlessof the degree of UAE. The serum creati-nine should be used to estimate glo-merular filtration rate (GFR) and stagethe level of chronic kidney disease(CKD), if present. (E)

Treatmentc In the treatment of the nonpregnant pa-tient with micro- or macroalbuminuria,

either ACE inhibitors or ARBs should beused. (A)

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

c Reduction of protein intake to 0.8–1.0g z kg body wt21 z day21 in individualswith diabetes and the earlier stages ofCKD and to 0.8 g z kg bodywt21 z day21

in the later stages of CKD may improvemeasures of renal function (UAE rate,GFR) and is recommended. (B)

c WhenACE inhibitors, ARBs, or diureticsare used, monitor serum creatinineand potassium levels for the develop-ment of increased creatinine and hy-perkalemia. (E)

c Continuedmonitoring of UAE to assessboth response to therapy and pro-gression of disease is reasonable. (E)

c When estimated GFR (eGFR) is ,60ml z min/1.73 m2

, evaluate and managepotential complications of CKD. (E)

c Consider referral to a physician ex-perienced in the care of kidney dis-ease for uncertainty about the etiologyof kidney disease, difficult manage-ment issues, or advanced kidney dis-ease. (B)

Retinopathy screening andtreatmentGeneral recommendationsc To reduce the risk or slow the pro-gression of retinopathy, optimize gly-cemic control. (A)

c To reduce the risk or slow the progres-sion of retinopathy, optimize blood pres-sure control. (A)

Screeningc Adults and children aged 10 years orolder with type 1 diabetes should havean initial dilated and comprehensiveeye examination by an ophthalmologistor optometrist within 5 years after theonset of diabetes. (B)

c 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)

c 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 ormore normal eye exams.Examinations will be required more fre-quently if retinopathy is progressing. (B)

c High-quality fundus photographs can de-tect most clinically significant diabetic


Executive Summary

retinopathy. Interpretation of the im-ages shouldbeperformedby a trained eyecare provider. While retinal photogra-phy may serve as a screening tool forretinopathy, it is not a substitute for acomprehensive eye exam, which shouldbe performed at least initially and at in-tervals thereafter as recommended byan eye care professional. (E)

c Women with preexisting diabetes whoare planning pregnancy or who havebecome pregnant should have a com-prehensive eye examination and shouldbe counseled on the risk of developmentand/or progression of diabetic retinopa-thy. Eye examination should occur inthe first trimester with close follow-upthroughout pregnancy and for 1 yearpostpartum. (B)

Treatmentc Promptly refer patients with any levelof macular edema, severe nonproli-ferative diabetic retinopathy (NPDR),or any PDR to an ophthalmologistwho is knowledgeable and experiencedin the management and treatment ofdiabetic retinopathy. (A)

c Laser photocoagulation therapy is in-dicated to reduce the risk of vision lossin patients with high-risk PDR, clini-cally significant macular edema, andsome cases of severe NPDR. (A)

c The presence of retinopathy is not acontraindication to aspirin therapy forcardioprotection, as this therapy doesnot increase the risk of retinal hemor-rhage. (A)

Neuropathy screening andtreatementc All patients should be screened fordistal symmetric polyneuropathy (DPN)starting at diagnosis of type 2 diabetesand 5 years after the diagnosis of type 1diabetes and at least annually thereafter,using simple clinical tests. (B)

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

c Screening for signs and symptoms ofcardiovascular autonomic neuropathyshould be instituted at diagnosis of type2 diabetes and 5 years after the diagnosisof type 1 diabetes. Special testing israrely needed and may not affect man-agement or outcomes. (E)

c Medications for the relief of specificsymptoms related to painful DPN andautonomic neuropathy are recom-mended, as they improve the quality oflife of the patient. (E)

Foot carec For all patients with diabetes, performan annual comprehensive foot exami-nation to identify risk factors predictiveof ulcers and amputations. The footexamination should include inspec-tion, assessment of foot pulses, andtesting for loss of protective sensation(10-g monofilament plus testing anyone of the following: vibration using128-Hz tuning fork, pinprick sensa-tion, ankle reflexes, or vibration per-ception threshold). (B)

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

c A multidisciplinary approach is rec-ommended for individuals with footulcers and high-risk feet, especiallythose with a history of prior ulcer oramputation. (B)

c 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)

c Initial screening for peripheral arterialdisease (PAD) should include a historyfor claudication and an assessment ofthe pedal pulses. Consider obtainingan ankle-brachial index (ABI), as manypatients with PAD are asymptomatic. (C)

c Refer patients with significant claudi-cation or a positive ABI for further vas-cular assessment and consider exercise,medications, and surgical options. (C)

Assessment of commoncomorbid conditionsc For patients with risk factors, signs orsymptoms, consider assessment and treat-ment for common diabetes-associatedconditions (see Table 15 of the “Stand-ards of Medical Care in Diabetesd2012”). (B)

Children and adolescentsGlycemic controlc Consider agewhen setting glycemic goalsin children and adolescents with type 1diabetes. (E)

Screening and managementof chronic complications inchildren and adolescentswith type 1 diabetesNephropathyc Annual screening for microalbuminuria,with a random spot urine sample foralbumin-to-creatinine ratio (ACR), shouldbe considered once the child is 10

years of age and has had diabetes for 5years. (B)

c Treatmentwith anACE inhibitor, titratedto normalization of albumin excretion,should be considered when elevatedACR is subsequently confirmed ontwo additional specimens from differ-ent days. (E)

Hypertensionc Initial treatment of high-normal bloodpressure (systolic or diastolic bloodpressure consistently above the 90th per-centile for age, sex, and height) includesdietary intervention and exercise, aimedat weight control and increased phys-ical activity, if appropriate. If targetblood pressure is not reached with 3–6months of lifestyle intervention, phar-macologic treatment should be consid-ered. (E)

c Pharmacologic treatment of hyper-tension (systolic or diastolic bloodpressure consistently above the 95thpercentile for age, sex, and height orconsistently .130/80 mmHg, if 95%exceeds that value) should be consid-ered as soon as the diagnosis is con-firmed. (E)

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

c 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)

DyslipidemiaScreeningc If there is a family history of hyper-cholesterolemia or a cardiovascularevent before age 55 years, or if familyhistory is unknown, then considerobtaining a fasting lipid profile onchildren .2 years of age soon afterdiagnosis (after glucose control hasbeen established). If family history isnot of concern, then consider the firstlipid screening at puberty ($10 years).For children diagnosed with diabetesat or after puberty, consider obtaininga fasting lipid profile soon after dia-gnosis (after glucose control has beenestablished). (E)

c For both age-groups, if lipids are abnor-mal, annual monitoring is reasonable. IfLDL cholesterol values are within theaccepted risk levels (,100 mg/dL [2.6mmol/l]), a lipid profile repeated every5 years is reasonable. (E)


Executive Summary

Treatmentc Initial therapy may consist of optimi-zation of glucose control and MNTusing a Step 2 American Heart Associ-ation Diet aimed at a decrease in theamount of saturated fat in the diet. (E)

c After the age of 10 years, the additionof a statin in patients who, after MNTand lifestyle changes, have LDL cho-lesterol .160 mg/dL (4.1 mmol/l), orLDL cholesterol . 30 mg/dL (3.4mmol/l) and one or more CVD riskfactors, is reasonable. (E)

c The goal of therapy is an LDL choles-terol value,100mg/dL (2.6mmol/l). (E)

Retinopathyc The first ophthalmologic examinationshould be obtained once the child is$10 years of age and has had diabetesfor 3–5 years. (B)

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

Celiac diseasec Consider screening children with type 1diabetes for celiac disease by measur-ing tissue transglutaminase or antiendo-mysial antibodies, with documentationof normal total serum IgA levels, soonafter the diagnosis of diabetes. (E)

c Testing should be considered in chil-dren with growth failure, failure to gainweight, weight loss, diarrhea, flatulence,abdominal pain, or signs of malabsorp-tion, or in children with frequent un-explained hypoglycemia or deteriorationin glycemic control. (E)

c Consider referral to a gastroenterolo-gist for evaluation with endoscopy andbiopsy for confirmation of celiac diseasein asymptomatic children with positiveantibodies. (E)

c 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. (B)

Hypothyroidismc Consider screening children with type 1diabetes for thyroid disease using thyroidperoxidase and thyroglobulin antibodiessoon after diagnosis. (E)

c Measuring TSH concentrations soonafter diagnosis of type 1 diabetes, aftermetabolic control has been established,is reasonable. If normal, consider re-checking every 1–2 years, especially

if the patient develops symptoms ofthyroid dysfunction, thyromegaly, oran abnormal growth rate. (E)

Transition from pediatric to adult carec As teens transition into emerging adult-hood, health care providers and familiesmust recognize their many vulnerabi-lities (B) and prepare the developingteen, beginning in early to mid adoles-cence and at least one year prior to thetransition. (E)

c Both pediatricians and adult health careproviders should assist in providing sup-port and links to resources for the teenand emerging adult. (B)

Preconception carec A1C levels should be as close tonormal aspossible (,7%) in an individual patientbefore conception is attempted. (B)

c Starting at puberty, preconception coun-seling should be incorporated in theroutine diabetes clinic visit for all womenof childbearing potential. (C)

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

c Medications used by suchwomen shouldbe evaluated prior to conception, sincedrugs commonly used to treat diabetesand its complications may be contra-indicated or not recommended in preg-nancy, including statins, ACE inhibitors,ARBs, andmost noninsulin therapies. (E)

c Since many pregnancies are unplanned,consider the potential risks and benefitsof medications that are contraindicatedin pregnancy in all women of childbear-ing potential, and counsel women usingsuch medications accordingly. (E)

Older adultsc Older adults who are functional, cog-nitively intact, and have significant lifeexpectancy should receive diabetes careusing goals developed for youngeradults. (E)

c Glycemic goals for older adults notmeeting the above criteria may be re-laxed using individual criteria, but hy-perglycemia leading to symptoms or riskof acute hyperglycemic complicationsshould be avoided in all patients. (E)

c Other cardiovascular risk factors shouldbe treated in older adults with consid-eration of the time frame of benefit andthe individual patient. Treatment of hy-pertension is indicated in virtually allolder adults, and lipid and aspirin therapy

may benefit those with life expectancy atleast equal to the time frame of primary orsecondary prevention trials. (E)

c Screening for diabetes complicationsshould be individualized in older adults,but particular attention should be paid tocomplications that would lead to func-tional impairment. (E)

Cystic fibrosis–relateddiabetes (CFRD)c Annual screening for CFRD with OGTTshould begin by age 10 years in all pa-tients with CF who do not have CFRD(B). Use of A1C as a screening test forCFRD is not recommended. (B)

c During a period of stable health thediagnosis of CFRD can be made in CFpatients according to usual diagnosticcriteria. (E)

c Patients with CFRD should be treatedwith insulin to attain individualized gly-cemic goals. (A)

c Annual monitoring for complicationsof diabetes is recommended, beginning5 years after the diagnosis of CFRD. (E)

Diabetes care in the hospitalc All patients with diabetes admitted to thehospital should have their diabetes clearlyidentified in the medical record. (E)

c All patients with diabetes should havean order for blood glucose monitoring,with results available to all membersof the health care team. (E)

c Goals for blood glucose levels:

○ Critically ill patients: Insulin ther-apy should be initiated for treatmentof persistent hyperglycemia startingat a threshold of no greater than 180mg/dL (10 mmol/L). Once insulintherapy is started, a glucose range of140–180 mg/dL (7.8 to 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 in-travenous insulin protocol that hasdemonstrated efficacy and safety inachieving the desired glucose rangewithout increasing risk for severehypoglycemia. (E)

○ Non–critically ill patients: There isno clear evidence for specific bloodglucose goals. If treated with in-sulin, premeal blood glucose targetsgenerally ,140 mg/dL (7.8 mmol/l)


Executive Summary

with random blood glucose ,180mg/dL (10.0 mmol/l) are reasonable,provided these targets can be safelyachieved. More stringent targetsmay be appropriate in stable pa-tients with previous tight glycemiccontrol. Less stringent targets may beappropriate in those with severe co-morbidites. (E)

c Scheduled subcutaneous insulin withbasal, nutritional, and correction com-ponents is the preferred method forachieving and maintaining glucose con-trol in noncritically ill patients.

c Glucose monitoring should be initi-ated in any patient not known to bediabetic who receives therapy associ-ated with high-risk for hyperglycemia,including high-dose glucocorticoidtherapy, initiation of enteral or parenteralnutrition, or other medications such as

octreotide or immunosuppressive medi-cations. (B) If hyperglycemia is docu-mented and persistent, consider treatingsuch patients to the same glycemic goalsas patients with known diabetes. (E)

c A hypoglycemia management protocolshould be adopted and implementedby each hospital or hospital system. Aplan for preventing and treating hy-poglycemia should be established foreach patient. Episodes of hypoglycemiain the hospital should be documentedin the medial record and tracked. (E)

c Consider obtaining an A1C on patientswith diabetes admitted to the hospitalif the result of testing in the previous2–3 months is not available. (E)

c Patients with hyperglycemia in thehospital who do not have a prior di-agnosis of diabetes should have ap-propriate plans for follow-up testingand care documented at discharge. (E)

Strategies for improving carec Care should be aligned with compo-nents of the Chronic Care Model toensure productive interactions be-tween a prepared proactive practiceteam and an informed activated pa-tient. (A)

c When feasible, care systems shouldsupport team-based care, communityinvolvement, patient registries, andembedded decision support tools tomeet patient needs. (B)

c Treatment decisions should be timelyand based on evidence-based guidelinesthat are tailored to individual patientpreferences, prognoses, and comorbid-ities. (B)

c A patient centered communication styleshould be employed that incorporatespatient preferences, assesses literacy andnumeracy, and addresses cultural bar-riers to care. (B)


Executive Summary

Standards ofMedical Care inDiabetesd2012

D iabetes mellitus is a chronic illnessthat requires continuing medical careand ongoing 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.A large body of evidence exists that sup-ports a range of interventions to improvediabetes outcomes.

These standards of care are intendedto provide clinicians, patients, researchers,payers, and other interested individualswith the components of diabetes care,general treatment goals, and tools to eval-uate the quality of care. While individualpreferences, comorbidities, and other pa-tient factors may require modification ofgoals, targets that are desirable for mostpatients with diabetes are provided. Spe-cifically titled sections of the standardsaddress children with diabetes, pregnantwomen, and people with prediabetes. Thesestandards are not intended to precludeclinical judgment or more extensive eval-uation and management of the patient byother specialists as needed. For more de-tailed information about management ofdiabetes, refer to references 1–3.

The recommendations included arescreening, diagnostic, and therapeutic ac-tions that are known or believed to favor-ably affect health outcomes of patients withdiabetes. A large number of these interven-tions have been shown to be cost-effective(4). A grading system (Table 1), developedby the American Diabetes Association(ADA) andmodeled after existingmethods,was utilized to clarify and codify the evi-dence that forms the basis for the recom-mendations. The level of evidence thatsupports each recommendation is listed af-ter each recommendation using the lettersA, B, C, or E.

These standards of care are revised an-nually by the ADA’s multidisciplinary Pro-fessional Practice Committee, incorporating

new evidence. For the current revision,committee members systematically searchedMedline for human studies related to eachsubsection and published since 1 January2010. Recommendations (bulleted at thebeginning of each subsection and also listedin the “Executive Summary: Standards ofMedical Care in Diabetesd2012”) were re-vised based on new evidence or, in somecases, to clarify the prior recommendationor match the strength of the wording tothe strength of the evidence. A table link-ing the changes in recommendations tonew evidence can be reviewed at http://professional.diabetes.org/CPR_Search.aspx. Subsequently, as is the case for allPosition Statements, the standards of carewere reviewed and approved by the Execu-tiveCommittee of ADA’s Board ofDirectors,which includes health care professionals,scientists, and lay people.

Feedback from the larger clinical com-munity was valuable for the 2012 revisionof the standards. Readers who wish tocomment on the “Standards of MedicalCare in Diabetesd2012” are invited to doso at http://professional.diabetes.org/CPR_Search.aspx.

Members of the Professional PracticeCommittee disclose all potential financialconflicts of interest with industry. Thesedisclosures were discussed at the onset ofthe standards revisionmeeting. Members ofthe committee, their employer, and theirdisclosed conflicts of interest are listed in the“Professional PracticeCommitteeMembers”table (see pg. S109). The AmericanDiabetesAssociation funds development of thestandards and all its position statementsout of its general revenues and does not uti-lize industry support for these purposes.

I. CLASSIFICATION ANDDIAGNOSIS

A. ClassificationThe classification of diabetes includes fourclinical classes:

c Type 1 diabetes (results from b-celldestruction, usually leading to absoluteinsulin deficiency)

c Type 2 diabetes (results from a pro-gressive insulin secretory defect on thebackground of insulin resistance)

c Other specific types of diabetes due toother causes, e.g., genetic defects in b-cellfunction, genetic defects in insulin action,diseases of the exocrine pancreas (such ascystic fibrosis), and drug- or chemical-induced (such as in the treatment ofHIV/AIDS or after organ transplantation)

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

Some patients cannot be clearly clas-sified as having type 1 or type 2 diabetes.Clinical presentation and disease progres-sion vary considerably in both types ofdiabetes. Occasionally, patients who oth-erwise have type 2 diabetes may presentwith ketoacidosis. Similarly, patients withtype 1may have a late onset and slow (butrelentless) progression of disease despitehaving features of autoimmune disease.Such difficulties in diagnosis may occurin children, adolescents, and adults. Thetrue diagnosis may become more obviousover time.

B. Diagnosis of diabetesRecommendationsFor decades, the diagnosis of diabetes wasbased on plasma glucose criteria, eitherthe fasting plasma glucose (FPG) or the2-h value in the 75-g oral glucose toler-ance test (OGTT) (5).

In 2009, an International Expert Com-mittee that included representatives of theAmerican Diabetes Association (ADA), theInternational Diabetes Federation (IDF),and the EuropeanAssociation for the Studyof Diabetes (EASD) recommended the useof the A1C test to diagnose diabetes,with a threshold of $6.5% (6), and ADAadopted this criterion in 2010 (5). The di-agnostic test should be performed using amethod that is certified by the NationalGlycohemoglobin Standardization Pro-gram (NGSP) and standardized or traceableto the Diabetes Control and ComplicationsTrial (DCCT) reference assay. Point-of-care


Originally approved 1988. Most recent review/revision October 2011.DOI: 10.2337/dc12-s011© 2012 by the American Diabetes Association. Readers may use this article as long as the work is properly



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

A1C assays, for which proficiency testing isnot mandated, are not sufficiently accurateat this time to use for diagnostic purposes.

Epidemiologic datasets show a similarrelationship between A1C and risk ofretinopathy as has been shown for thecorresponding FPG and 2-h PG thresholds.The A1C has several advantages to the FPGand OGTT, including greater convenience(since fasting is not required), evidence tosuggest greater preanalytical stability, andless day-to-day perturbations during pe-riods of stress and illness. These advan-tages must be balanced by greater cost,the limited availability of A1C testing incertain regions of the developing world,and the incomplete correlation betweenA1C and average glucose in certain indi-viduals. In addition, HbA1c levelsmay varywith patients’ race/ethnicity (7,8). Somehave posited that glycation rates differ byrace (with, for example, African Americanshaving higher rates of glycation), but thisis controversial. A recent epidemiologicstudy found that, when matched for FPG,African Americans (with and without di-abetes) indeed had higher A1C thanwhites, but also had higher levels of fruc-tosamine and glycated albumin and lowerlevels of 1,5-anhydroglucitol, suggestingthat their glycemic burden (particularly

postprandially) may be higher (9). Epide-miologic studies forming the frameworkfor recommending use of the A1C to diag-nose diabetes have all been in adult popu-lations. Whether the cut point would bethe same to diagnose children with type 2diabetes is an area of uncertainty (10). A1Cinaccurately reflects glycemia with certainanemias and hemoglobinopathies. For pa-tients with an abnormal hemoglobin butnormal red cell turnover, such as sickle celltrait, anA1Cassaywithout interference fromabnormal hemoglobins should be used (anupdated list is available at www.ngsp.org/npsp.org/interf.asp). For conditionswith ab-normal red cell turnover, such as pregnancy,recent blood loss or transfusion, or someanemias, 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. Analysesof National Health and Nutrition Exami-nation Survey (NHANES) data indicatethat, assuming universal screening ofthe undiagnosed, the A1C cut point of$6.5% identifies one-third fewer cases

of undiagnosed diabetes than a fastingglucose cut point of $126 mg/dL (7.0mmol/L) (11). However, in practice, alarge portion of the diabetic populationremains unaware of their condition.Thus, the lower sensitivity of A1C at thedesignated cut point may well be offset bythe test’s greater practicality, and widerapplication of a more convenient test(A1C) may actually increase the numberof diagnoses made.

As with most diagnostic tests, a testresult diagnostic of diabetes should berepeated to rule out laboratory error, unlessthe diagnosis is clear on clinical grounds,such as a patient with a hyperglycemiccrisis or classic symptoms of hyperglycemiaand a randomplasma glucose$200mg/dL.It is preferable that the same test be repeatedfor confirmation, since therewill be a greaterlikelihood of concurrence in this case. Forexample, if the A1C is 7.0% and a repeatresult is 6.8%, the diagnosis of diabetes isconfirmed. However, if two different tests(such as A1C and FPG) are both above thediagnostic thresholds, the diagnosis of dia-betes is also confirmed.

On the other hand, if two differenttests are available in an individual andthe results are discordant, the test whoseresult 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 diabetescriterion of the A1C (two results $6.5%)but not the FPG (,126 mg/dL or 7.0mmol/L), or vice versa, that person shouldbe considered to have diabetes.

Table 1dADA evidence grading system for clinical practice recommendations

Level ofevidence Description

A Clear evidence from well-conducted, generalizable, RCTs that are adequatelypowered, including:

c Evidence from a well-conducted multicenter trial

c Evidence from a meta-analysis that incorporated quality ratings in the analysisCompelling nonexperimental evidence, i.e., “all or none” rule developedby Center for Evidence Based Medicine at Oxford

Supportive evidence from well-conducted randomized controlled trials thatare adequately powered, including:

c Evidence from a well-conducted trial at one or more institutions

c Evidence from a meta-analysis that incorporated quality ratings inthe analysis

B Supportive evidence from well-conducted cohort studiesc Evidence from a well-conducted prospective cohort study or registry

c Evidence from a well-conducted meta-analysis of cohort studiesSupportive evidence from a well-conducted case-control study

C Supportive evidence from poorly controlled or uncontrolled studiesc Evidence from RCTs with one or more major or three or moreminor methodological flaws that could invalidate the results

c Evidence from observational studies with high potential for bias(such as case series with comparison with historical controls)

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

E Expert consensus or clinical experience

Table 2dCriteria for the diagnosis ofdiabetes

A1C $6.5%. The test should be performedin a laboratory using a method that is NGSPcertified and standardized to the DCCTassay.*

ORFPG $126 mg/dL (7.0 mmol/L). Fasting isdefined as no caloric intake for at least 8 h.*

OR2-h plasma glucose$200mg/dL (11.1mmol/L)during an OGTT. The test should beperformed as described by the WHO, usinga glucose load containing the equivalent of75 g anhydrous glucose dissolved in water.*

ORIn a patient with classic symptoms ofhyperglycemia or hyperglycemic crisis,a random plasma glucose $200 mg/dL(11.1 mmol/L)

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


Position Statement

Since there is preanalytic and analyticvariability 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 health care professionalmight opt to follow the patient closely andrepeat the testing in 3–6 months. The cur-rent diagnostic criteria for diabetes aresummarized in Table 2.

C. Categories of increased risk fordiabetes (prediabetes)In 1997 and 2003, The Expert Committeeon Diagnosis and Classification of DiabetesMellitus (12,13) 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 mg/dL [5.6mmol/L] to 125 mg/dL [6.9 mmol/L]),or impaired glucose tolerance (IGT) (2-hvalues in the OGTT of 140 mg/dL [7.8mmol/L] to 199 mg/dL [11.0 mmol/L]). Itshould be noted that the World HealthOrganization (WHO) and a number ofother diabetes organizations define the cut-off for IFG at 110 mg/dL (6.1 mmol/L).

Individuals with IFG and/or IGT havebeen referred to as having prediabetes,indicating the relatively high risk for thefuture development of diabetes. IFG andIGT should not be viewed as clinicalentities in their own right but rather riskfactors for diabetes aswell as cardiovasculardisease (CVD). IFG and IGT are associatedwith obesity (especially abdominal or vis-ceral obesity), dyslipidemia with high tri-glycerides and/or lowHDL cholesterol, andhypertension.

As is the case with the glucose meas-ures, several prospective studies that usedA1C to predict the progression to diabetesdemonstrated a strong, continuous asso-ciation between A1C and subsequent di-abetes. In a systematic review of 44,203individuals from 16 cohort studies with afollow-up interval averaging 5.6 years(range 2.8-12 years), those with an A1Cbetween 5.5 and 6.0% had a substantiallyincreased risk of diabetes with 5-year in-cidences ranging from 9–25%. An A1Crange of 6.0 to 6.5% had a 5-year risk ofdeveloping diabetes between 25 to 50%and relative risk 20 times higher compared

with anA1Cof 5.0% (14). In a community-based study of black andwhite adults with-out diabetes, baseline A1C was a strongerpredictor of subsequent diabetes and car-diovascular events than fasting glucose(15). Other analyses suggest that an A1Cof 5.7% is associatedwith diabetes risk sim-ilar to that of the high-risk participants inthe Diabetes Prevention Program (DPP).

Hence, it is reasonable to consider anA1C range of 5.7 to 6.4% as identifyingindividuals with high risk for futurediabetes, a state that may be referred toas prediabetes (5). As is the case for indi-viduals found to have IFG and IGT, indi-viduals with an A1C of 5.7–6.4% shouldbe informed of their increased risk for di-abetes as well as CVD and counseledabout effective strategies to lower theirrisks (see section IV. PREVENTION/DELAY OF TYPE 2 DIABETES). As withglucose measurements, the continuum ofrisk is curvilinear, so that as A1C rises therisk of diabetes rises disproportionately(14). Accordingly, interventions shouldbe most intensive and follow-up shouldbe particularly vigilant for those withA1Cs .6.0%, who should be consideredto be at very high risk. Table 3 summarizesthe categories of increased risk for diabetes.

II. TESTING FOR DIABETES INASYMPTOMATIC PATIENTS

Recommendationsc Testing to detect type 2 diabetes andassess 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 begin atage 45 years. (B)

c If tests are normal, repeat testing at leastat 3-year intervals is reasonable. (E)

c To test for diabetes or to assess riskof future diabetes, the A1C, FPG, or 2-h75-g OGTT are appropriate. (B)

c In those identified with increased riskfor future diabetes, identify and, if appro-priate, treat other CVD risk factors. (B)

For many illnesses, there is a majordistinction between screening and diag-nostic testing. However, for diabetes, thesame tests would be used for “screening”as for diagnosis. Diabetes may be identifiedanywhere along a spectrum of clinical sce-narios ranging from a seemingly low-riskindividual who happens to have glucosetesting, to a higher-risk individual whom

the provider tests because of high suspicionof diabetes, to the symptomatic patient.The discussion herein is primarily framedas testing for diabetes in those withoutsymptoms. The same assays used for test-ing for diabetes will also detect individualswith prediabetes.

A. Testing for type 2 diabetes andrisk of future diabetes in adultsPrediabetes and diabetes meet establishedcriteria for conditions in which early de-tection is appropriate. Both conditions arecommon, increasing in prevalence, andimpose significant public health burdens.There is a long presymptomatic phasebefore the diagnosis of type 2 diabetes isusually made. Relatively simple tests areavailable to detect preclinical disease. Ad-ditionally, the duration of glycemic burdenis a strong predictor of adverse outcomes,and effective interventions exist to preventprogression of prediabetes to diabetes (seesection IV. PREVENTION/DELAY OFTYPE 2 DIABETES) and to reduce risk ofcomplications of diabetes (see section V.I.PREVENTION AND MANAGEMENT OFDIABETES COMPLICATIONS).

Type 2 diabetes is frequently notdiagnosed until complications appear,and approximately one-fourth of all peoplewith diabetes in the U.S. may be undiag-nosed. The effectiveness of early identifica-tion of prediabetes and diabetes throughmass testing of asymptomatic individualshas not been proven definitively, andrigorous trials to provide such proof areunlikely to occur. In a large randomizedcontrolled trial (RCT) in Europe, generalpractice patients between the ages of 40and 69 years were screened for diabetesand then randomized by practice to routinecare of diabetes or intensive treatment ofmultiple risk factors. After 5.3 years offollow-up, CVD risk factors were modestlybut significantly more improved with in-tensive treatment. Incidence of first CVD

Table 3dCategories of increased risk fordiabetes (prediabetes)*

FPG 100 mg/dL (5.6 mmol/L) to 125 mg/dL(6.9 mmol/L) (IFG)

OR2-h plasma glucose in the 75-g OGTT140 mg/dL (7.8 mmol/L) to 199 mg/dL(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 the range.


Position Statement

event and mortality rates were not signifi-cantly different between groups (16). Thisstudy would seem to add support for earlytreatment of screen-detected diabetes, asrisk factor control was excellent even inthe routine treatment arm and both groupshad lower event rates than predicted. Theabsence of a control unscreened arm limitsthe ability to definitely prove that screeningimpacts outcomes. Mathematical modelingstudies suggest that screening independentof risk factors beginning at age 30 or age 45years is highly cost-effective (,$11,000per quality-adjusted life-year gained) (17).

Recommendations for testing for di-abetes 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. There iscompelling evidence that lower BMI cutpoints suggest diabetes risk in some racialand ethnic groups. In a large multiethniccohort study, for an equivalent incidencerate of diabetes conferred by a BMI of 30kg/m2 in whites, the BMI cutoff value was24 kg/m2 in South Asians, 25 kg/m2 inChinese, and 26 kg/m2 African Americans(18).Disparities in screening rates, not ex-plainable by insurance status, are high-lighted by evidence that despite muchhigher prevalence of type 2 diabetes,non-Caucasians in an insured populationare no more likely than Caucasians to bescreened for diabetes (19). Because ageis a major risk factor for diabetes, testingof those without other risk factors shouldbegin no later than age 45 years.

Either A1C, FPG, or the 2-h OGTT isappropriate for testing. It should be notedthat the tests do not necessarily detectdiabetes in the same individuals. The ef-ficacy of interventions for primary pre-vention of type 2 diabetes (20–26) hasprimarily been demonstrated among in-dividuals with IGT, not for individualswith isolated IFG or for individuals withspecific A1C levels.

The appropriate interval betweentests is not known (27). The rationalefor the 3-year interval is that false nega-tives will be repeated before substantialtime elapses, and there is little likelihoodthat an individual will develop significantcomplications of diabetes within 3 yearsof a negative test result. In the modelingstudy, repeat screening every 3 or 5 yearswas cost-effective (17).

Because of the need for follow-up anddiscussion of abnormal results, testingshould be carried out within the healthcare setting. Community screening outsidea health care setting is not recommendedbecause people with positive tests may notseek, or have access to, appropriate follow-up testing and care. Conversely, there maybe failure to ensure appropriate repeattesting for individuals who test negative.Community screening may also be poorlytargeted, i.e., it may fail to reach the groupsmost at risk and inappropriately test thoseat low risk (the worried well) or even thosealready diagnosed.

B. Testing for type 2 diabetesin childrenThe incidence of type 2 diabetes in ado-lescents has increased dramatically in thelast decade, especially in minority popu-lations (28), although the disease remainsrare in the general pediatric population(29). 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 healthcare setting (30).The recommendations of the ADA con-sensus statement on Type 2 Diabetes inChildren and Youth, with some modifica-tions, are summarized in Table 5 (30).

C. Screening for type 1 diabetesGenerally, people with type 1 diabetespresent with acute symptoms of diabetesand markedly elevated blood glucoselevels, and most cases are diagnosed soonafter the onset of hyperglycemia. However,evidence from type 1 prevention studiessuggests that measurement of islet auto-antibodies identifies individuals who are atrisk for developing type 1 diabetes. Suchtesting may be appropriate in high-risk

Table 4dCriteria for testing for diabetes in asymptomatic adult individuals

1. Testing should be considered in all adults who are overweight (BMI $25 kg/m2*) and whohave one or more additional risk factors:c physical inactivity

c first-degree relative with diabetes

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

c women who delivered a baby weighing .9 lb or who were diagnosed with GDM

c hypertension (blood pressure $140/90 mmHg or on therapy for hypertension)

c HDL cholesterol level ,35 mg/dL (0.90 mmol/L) and/or a triglyceride level .250 mg/dL(2.82 mmol/L)

c women with PCOS

c A1C $5.7%, IGT, or IFG on previous testing

c other clinical conditions associated with insulin resistance (e.g., severe obesity, acanthosisnigricans)

c history of CVD

2. In the absence of the above criteria, testing for diabetes should begin at age 45 years3. If results are normal, testing should be repeated at least at 3-year intervals, with considerationof more-frequent testing depending on initial results (e.g., those with prediabetes should betested yearly) and risk status.

*At-risk BMI may be lower in some ethnic groups. PCOS, polycystic ovary syndrome.

Table 5dTesting for type 2 diabetes in asymptomatic children

Criteriac Overweight (BMI .85th percentile for age and sex, weight for height .85thpercentile, or weight .120% of ideal for height

Plus any two of the following risk factors:c Family history of type 2 diabetes in first- or second-degree relative

c Race/ethnicity (Native American, African American, Latino, Asian American,Pacific Islander)

c Signs of insulin resistance or conditions associated with insulin resistance(acanthosis nigricans, hypertension, dyslipidemia, PCOS, or birth weight small forgestational age birthweight)

c Maternal history of diabetes or GDM during the child’s gestationAge of initiation: 10 years or at onset of puberty, if puberty occurs at a younger ageFrequency: every 3 years

PCOS, polycystic ovary syndrome


Position Statement

individuals, such as those with prior tran-sient hyperglycemia or those who haverelativeswith type 1 diabetes, in the contextof clinical research studies (see, e.g., http://www2.diabetestrialnet.org). Widespreadclinical testing of asymptomatic low-risk in-dividuals cannot currently be recommended,as it would identify very few individuals inthe general population who are at risk. In-dividuals who screen positive should becounseled about their risk of developing di-abetes. Clinical studies are being conductedto test variousmethods of preventing type 1diabetes, or reversing early type 1 diabetes,in those with evidence of autoimmunity.

III. DETECTION ANDDIAGNOSIS OF GESTATIONALDIABETES MELLITUS (GDM)

Recommendationsc Screen for undiagnosed type 2 diabetesat thefirst prenatal visit in thosewith riskfactors, using standard diagnostic crite-ria. (B)

c In pregnant women not previouslyknown to have diabetes, screen for GDMat 24–28 weeks’ gestation, using a 75-g2-h OGTT and the diagnostic cut pointsin Table 6. (B)

c Screen women with GDM for persistentdiabetes at 6–12 weeks’ postpartum,using a test other than A1C. (E)

c Women with a history of GDM shouldhave lifelong screening for the devel-opment of diabetes or prediabetes atleast every 3 years. (B)

c Women with a history of GDM foundto have prediabetes should receive life-style interventions or metformin to pre-vent diabetes. (A)

For many years, GDM was defined asany degree of glucose intolerance with

onset or first recognition during preg-nancy (12), whether or not the conditionpersisted after pregnancy, and not exclud-ing the possibility that unrecognized glu-cose intolerance may have antedated orbegun concomitantly with the pregnancy.This definition facilitated a uniform strat-egy for detection and classification ofGDM,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(31). Because of this, it is reasonable toscreen women with risk factors for type 2diabetes (Table 4) for diabetes at their initialprenatal visit, using standard diagnosticcriteria (Table 2). Women found to havediabetes at this visit should receive a di-agnosis of overt, not gestational, diabetes.

GDM carries risks for the mother andneonate. The Hyperglycemia and AdversePregnancyOutcomes (HAPO) study (32), alarge-scale (;25,000 pregnant women)multinational epidemiologic study, dem-onstrated that risk of adverse maternal, fe-tal, and neonatal outcomes continuouslyincreased as a function of maternal glyce-mia at 24–28 weeks, even within rangespreviously considered normal for preg-nancy. For most complications, there wasno threshold for risk. These results have ledto careful reconsideration of the diagnosticcriteria for GDM. After deliberations in2008–2009, the International Associationof Diabetes and Pregnancy Study Groups(IADPSG), an international consensusgroup with representatives from multipleobstetrical and diabetes organizations, in-cluding ADA, developed revised recom-mendations for diagnosing GDM. Thegroup recommended that all women notknown to have prior diabetes undergo a75-g OGTT at 24–28 weeks of gestation.Additionally, the group developed diag-nostic cut points for the fasting, 1-h, and2-h plasma glucose measurements thatconveyed an odds ratio for adverse out-comes of at least 1.75 compared withwomen with the mean glucose levels inthe HAPO study. Current screening anddiagnostic strategies, based on the IADPSGstatement (33), 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.ADA recognizes the anticipated signifi-cant increase in the incidence of GDMdiagnosed by these criteria and is sensitiveto concerns about the “medicalization” of

pregnancies previously categorized asnormal. These diagnostic criteria changesare being made in the context of worri-some worldwide increases in obesity anddiabetes rates, with the intent of optimiz-ing gestational outcomes for women andtheir 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).However, there is emerg-ing observational and retrospective evi-dence that women diagnosed with thenew criteria (even if they would not havebeen diagnosed with older criteria) haveincreased rates of poor pregnancy outcomessimilar to those of women with GDM byprior criteria (34,35). Expected benefitsto these pregnancies and offspring is infer-red from intervention trials that focused onwomen with more mild hyperglycemiathan identified using olderGDMdiagnosticcriteria and that found modest benefits(36,37). The frequency of follow-up andblood glucose monitoring for these womenis not yet clear but likely to be less intensivethan for women diagnosed by the older cri-teria. It is important to note that 80–90%ofwomen in both of the mild GDM studies(whose glucose values overlapped with thethresholds recommended herein) could bemanaged with lifestyle therapy alone.

The American College of Obstetricsand Gynecology announced in 2011 thatthey continue to recommend use of priordiagnostic criteria for GDM (38). Severalother countries have adopted the new cri-teria, and a report from the WHO on thistopic is pending at the time of the publi-cation of these standards.

Because some cases of GDMmay rep-resent preexisting undiagnosed type 2diabetes, women with a history of GDMshould be screened for diabetes 6–12weeks’ postpartum, using nonpregnantOGTT criteria. Because of their prepartumtreatment for hyperglycemia, use of theA1C for diagnosis of persistent diabetes atthe postpartum visit is not recommended(39).Womenwith a history of GDMhave agreatly increased subsequent risk for diabe-tes (40) and should be followed up withsubsequent screening for the developmentof diabetes or prediabetes, as outlined insection II. TESTING FOR DIABETES INASYMPTOMATIC PATIENTS.

Lifestyle interventions or metforminshould be offered to womenwith a history

Table 6dScreening for and diagnosis ofGDM

Perform a 75-g OGTT, with plasma glucosemeasurement fasting and at 1 and 2 h, at24–28 weeks’ gestation in women notpreviously diagnosed with overt diabetes.

The OGTT should be performed in themorning after an overnight fast of at least8 h.

The diagnosis of GDM is made when any ofthe following plasma glucose values areexceeded:c Fasting $92 mg/dL (5.1 mmol/L)

c 1 h $180 mg/dL (10.0 mmol/L)

c 2 h $153 mg/dL (8.5 mmol/L)


Position Statement

of GDM who develop prediabetes, asdiscussed in section IV. PREVENTION/DELAY OF TYPE 2 DIABETES.

IV. PREVENTION/DELAYOF TYPE 2 DIABETES

Recommendationsc Patientswith IGT (A), IFG (E), or anA1Cof 5.7–6.4% (E) should be referred to aneffective ongoing support program tar-geting weight loss of 7% of body weightand increasing physical activity to at least150 min per week of moderate activitysuch as walking.

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

c Based on the cost-effectiveness of dia-betes prevention, such programs shouldbe covered by third-party payers. (B)

c Metformin therapy for prevention oftype 2 diabetes may be considered inthose with IGT (A), IFG (E), or an A1Cof 5.7–6.4% (E), especially for those withBMI .35 kg/m2, age ,60 years, andwomen with prior GDM. (A)

c At least annual monitoring for the de-velopment of diabetes in those withprediabetes is suggested. (E)

RCTs have shown that individuals athigh risk for developing type 2 diabetes(those with IFG, IGT, or both) can signif-icantly decrease the rate of onset of diabeteswith particular interventions (20–26).These include intensive lifestyle modifica-tion programs that have been shown tobe very effective (;58% reduction after3 years) and use of the pharmacologicagents metformin, a glucosidase inhibi-tors, orlistat, and thiazolidinediones,each of which has been shown to decreaseincident diabetes to various degrees. Follow-up of three large studies of lifestyle inter-vention has shown sustained reduction inthe rate of conversion to type 2 diabetes,with 43% reduction at 20 years in the DaQing study (41), 43% reduction at 7 yearsin the Finnish Diabetes Prevention Study(DPS) (42), and 34% reduction at 10years in the U.S. Diabetes Prevention Pro-gram Outcome Study (DPPOS) (43). Acost-effectiveness model suggested thatlifestyle interventions as delivered in theDPP are cost-effective (44), and actualcost data from the DPP and DPPOS con-firm that lifestyle interventions are highlycost-effective (45). Group delivery of theDPP intervention in community settingshas the potential to be significantly lessexpensive while still achieving similarweight loss (46).

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% weightloss and moderate physical activity of atleast 150 min per week). Regarding drugtherapy for diabetes prevention, a consen-sus panel felt that metformin should bethe only drug considered (47). For otherdrugs, issues of cost, side effects, and lackof persistence of effect in some studies(48) require consideration. Metforminwas less effective than lifestyle interven-tion in the DPP and DPPOS but may becost-saving over a 10-year period (45). Itwas as effective as lifestyle in participantswith a BMI of at least 35 kg/m2 (20), andin women with a history of GDM, metfor-min and intensive lifestyle led to an equiv-alent 50% reduction in the risk of diabetes(49). Metformin therefore might reason-ably be recommended for very-high-riskindividuals (those with a history of GDM,the very obese, and/or those with moresevere or progressive hyperglycemia). Ofnote in the DPP, metformin was not sig-nificantly better than placebo in thoseover 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 patientswith established diabetes,assist in formulating a management plan,and provide a basis for continuing care.Laboratory tests appropriate to the evalua-tion of each patient’s medical conditionshould be performed. A focus on the com-ponents of comprehensive care (Table 7)will assist the health care team to ensureoptimal management of the patient withdiabetes.

B. ManagementPeople with diabetes should receive med-ical care from a physician-coordinatedteam. Such teams may include, but arenot limited to, physicians, nurse practition-ers, physician’s assistants, nurses, dietitians,pharmacists, and mental health professio-nals with expertise and a special interest indiabetes. It is essential in this collaborativeand integrated team approach that individ-uals with diabetes assume an active role intheir care.

The management plan should beformulated as a collaborative therapeuticalliance among the patient and family,the physician, and other members of thehealth care team. A variety of strategiesand techniques should be used to provideadequate education and developmentof problem-solving skills in the variousaspects of diabetes management. Imple-mentation of the management plan re-quires that each aspect is understood andagreed to by the patient and the careproviders and that the goals and treatmentplan are reasonable. Any plan should rec-ognize diabetes self-management education(DSME) and on-going diabetes support asan integral component of care. In develop-ing the plan, consideration should be givento the patient’s age, school orwork scheduleand conditions, physical activity, eatingpatterns, social situation and cultural fac-tors, and presence of complications ofdiabetes or other medical conditions.

C. Glycemic control1. Assessment of glycemic control. Twoprimary techniques are available for healthproviders and patients to assess the ef-fectiveness of the management plan onglycemic control: patient self-monitoring ofblood glucose (SMBG) or interstitial glu-cose, and A1C.

a. Glucose monitoringRecommendationsc SMBG should be carried out three ormore times daily for patients using mul-tiple insulin injections or insulin pumptherapy. (B)

c For patients using less-frequent in-sulin injections, noninsulin therapies,or medical nutrition therapy (MNT)alone, SMBG may be useful as a guideto management. (E)

c To achieve postprandial glucose targets,postprandial SMBGmay be appropriate.(E)

c 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)

c 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)

c Although the evidence for A1C-loweringis less strong in children, teens, andyounger adults, CGM may be helpful inthese groups. Success correlates with ad-herence to ongoing use of the device. (C)


Position Statement

c CGM may be a supplemental tool toSMBG in those with hypoglycemiaunawareness and/or frequent hypogly-cemic episodes. (E)

Major clinical trials of insulin-treatedpatients that demonstrated the benefitsof intensive glycemic control on diabetescomplications have included SMBG as partof multifactorial interventions, suggesting

that SMBG is a component of effectivetherapy. SMBG allows patients to evaluatetheir individual response to therapy andassess whether glycemic targets are beingachieved. Results of SMBG can be usefulin preventing hypoglycemia and adjustingmedications (particularly prandial insulindoses), MNT, and physical activity.

The frequency and timing of SMBGshould be dictated by the particular needs

and goals of the patient. SMBG is espe-cially important for patients treated withinsulin to monitor for and prevent asymp-tomatic hypoglycemia and hyperglycemia.For most patients with type 1 diabetes andpregnant women taking insulin, SMBG isrecommended three or more times daily.For these populations, significantly morefrequent testing may be required to reachA1C targets safely without hypoglycemiaand for hypoglycemia detection prior tocritical tasks such as driving. In a largedatabase study of almost 27,000 childrenand adolescents with type 1 diabetes, afteradjustment for multiple confounders, in-creased daily frequency of SMBG wassignificantly associated with lower A1C(20.2% per additional test per day, level-ing off at 5 tests per day) and with feweracute complications (50). The optimal fre-quency and timing of SMBG for patientswith type 2 diabetes on noninsulin therapyis unclear. A meta-analysis of SMBG innon–insulin-treated patients with type 2diabetes concluded that some regimens ofSMBG were associated with a reduction inA1C of 20.4%. However, many of thestudies 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 (51). Several randomized trialshave called into question the clinical utilityand cost-effectiveness of routine SMBG innon–insulin-treated patients (52–54).

Because the accuracy of SMBG isinstrument and user dependent (55), itis important to evaluate each patient’smonitoring technique, both initially andat regular intervals thereafter. In addition,optimal use of SMBG requires proper in-terpretation of the data. Patients should betaught how to use the data to adjust foodintake, exercise, or pharmacological ther-apy to achieve specific glycemic goals,and these skills should be reevaluated pe-riodically.

Real-time CGM through the measure-ment of interstitial glucose (which corre-lates well with plasma glucose) is available.These sensors require calibration withSMBG, and the latter are still recommendedfor making acute treatment decisions.CGM devices have alarms for hypo- andhyperglycemic excursions. Small studiesin selected patients with type 1 diabeteshave suggested that CGM use reduces thetime spent in hypo- and hyperglycemicranges andmaymodestly improve glycemiccontrol. A 26-week randomized trial of 322type 1 patients showed that adults age 25

Table 7dComponents of the comprehensive diabetes evaluation

Medical historyc Age and characteristics of onset of diabetes (e.g., DKA, asymptomatic laboratory finding)

c Eating patterns, physical activity habits, nutritional status, and weight history;growth and development in children and adolescents

c Diabetes education history

c Review of previous treatment regimens and response to therapy (A1C records)

c Current treatment of diabetes, including medications and medication adherence,meal plan, physical activity patterns, and readiness for behavior change

c Results of glucose monitoring and patient’s use of data

c DKA frequency, severity, and cause

c Hypoglycemic episodes

○ Hypoglycemia awareness○ Any severe hypoglycemia: frequency and cause

c History of diabetes-related complications

○ Microvascular: retinopathy, nephropathy, neuropathy (sensory, including historyof foot lesions; autonomic, including sexual dysfunction and gastroparesis)

○ Macrovascular: CHD, cerebrovascular disease, PAD○ Other: psychosocial problems,* dental disease*

Physical examinationc Height, weight, BMI

c Blood pressure determination, including orthostatic measurements when indicated

c Fundoscopic examination*

c Thyroid palpation

c Skin examination (for acanthosis nigricans and insulin injection sites)

c 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 evaluationc A1C, if results not available within past 2–3 months

c If not performed/available within past year:

○ Fasting lipid profile, including total, LDL, and HDL cholesterol and triglycerides○ Liver function tests○ Test for UAE with spot urine albumin-to-creatinine ratio○ Serum creatinine and calculated GFR○ Thyroid-stimulating hormone in type 1 diabetes, dyslipidemia, or women overage 50 years

Referralsc Eye care professional for annual dilated eye exam

c Family planning for women of reproductive age

c Registered dietitian for MNT

c DMSE

c Dentist for comprehensive periodontal examination

c Mental health professional, if needed*See appropriate referrals for these categories.


Position Statement

years and older using intensive insulintherapy and CGM experienced a 0.5% re-duction in A1C (from ;7.6–7.1%) com-pared with usual intensive insulin therapywith SMBG (56). Sensor use in children,teens, and adults to age 24 years did notresult in significant A1C lowering, and therewas no significant difference in hypoglyce-mia in any group. Importantly, the greatestpredictor of A1C lowering in this study forall age-groups was frequency of sensor use,which was lower in younger age-groups.In a smaller RCT of 129 adults and childrenwith baseline A1C,7.0%, outcomes com-bining A1C and hypoglycemia favored thegroup utilizing CGM, suggesting that CGMis also beneficial for individuals with type 1diabetes who have already achieved excel-lent control (57).

A recent RCT of 120 children andadults with type 1 diabetes with baselineA1C ,7.5% showed that real-time CGMwas associated with reduced time spent inhypoglycemia and a small but significantdecrease in A1C compared with blindedCGM (58). A trial comparing CGM plusinsulin pump to SMBG plus multiple in-jections of insulin in adults and childrenwith type 1 diabetes showed significantlygreater improvements in A1C with “sen-sor augmented pump” therapy (59,60),but this trial did not isolate the effect ofCGM itself. Although CGM is an evolvingtechnology, these data suggest that, in ap-propriately selected patients who are mo-tivated to wear it most of the time, it mayoffer benefit. CGM may be particularlyuseful in those with hypoglycemia un-awareness and/or frequent episodes of hy-poglycemia, and studies in this area areongoing. CGM forms the underpinningfor the development of pumps that sus-pend insulin delivery when hypoglycemiais developing as well as for the burgeoningwork on “artificial pancreas” systems.

b. A1CRecommendationsc Perform the A1C test at least two times ayear in patients who are meeting treat-ment goals (and who have stable glyce-mic control). (E)

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

c Use of point-of-care (POC) testing forA1C provides the opportunity for moretimely treatment changes. (E)

Because A1C is thought to reflectaverage glycemia over several months(55), and has strong predictive value for

diabetes complications (61,62), A1C test-ing should be performed routinely in allpatients 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 maintained.For any individual patient, the frequency ofA1C testing should be dependent on theclinical situation, the treatment regimenused, and the judgment of the clinician.Some patients with stable glycemia wellwithin target may do well with testingonly twice per year, while unstable orhighly intensively managed patients(e.g., pregnant type 1 women) may betested more frequently than every 3months. The availability of the A1C resultat the time that the patient is seen (POCtesting) has been reported in small studiesto result in increased intensification oftherapy and improvement in glycemiccontrol (63,64). However, two recent sys-tematic reviews and meta-analyses foundno significant difference in A1C betweenPOC and laboratory A1C usage (65,66).

The A1C test is subject to certainlimitations. Conditions that affect eryth-rocyte turnover (hemolysis, blood loss)and hemoglobin variants must be consid-ered, particularly when the A1C resultdoes not correlate with the patient’s clinicalsituation (55). In addition, A1C does notprovide ameasure of glycemic variability orhypoglycemia. For patients prone to glyce-mic variability (especially type 1 patients,or type 2 patients with severe insulin de-ficiency), glycemic control is best judgedbythe combination of results of SMBG testingand the A1C. The A1C may also serve as acheck on the accuracy of the patient’smeter(or the patient’s reported SMBG results)and the adequacy of the SMBG testingschedule.

Table 8 contains the correlation be-tween A1C levels andmeanplasma glucoselevels based on data from the internationalA1C-Derived Average Glucose (ADAG) tri-al utilizing frequent SMBG and CGM in507 adults (83% Caucasian) with type 1,type 2, and no diabetes (67). ADA and theAmerican Association of Clinical Chemistshave determined that the correlation (r 50.92) is strong enough to justify reportingboth an A1C result and an estimated aver-age glucose (eAG) result when a clinicianorders the A1C test. The table in pre-2009versions of the “Standards of Medical Carein Diabetes” describing the correlation be-tween A1C and mean glucose was derivedfrom relatively sparse data (one 7-pointprofile over 1 day per A1C reading) in the

primarily Caucasian type 1 participants inthe DCCT (68). Clinicians should note thatthe numbers in the table are now different,as they are based on ;2,800 readings perA1C in the ADAG trial.

In the ADAG study, there were no sig-nificant differences among racial and ethnicgroups in the regression lines between A1Cand mean glucose, although there was atrend toward a difference between African/African American and Caucasian partici-pants. A small study comparing A1C toCGM data in type 1 children found ahighly statistically significant correlationbetween A1C and mean blood glucose,although the correlation (r 5 0.7) was sig-nificantly lower than in theADAG trial (69).Whether there are significant differences inhow A1C relates to average glucose in chil-dren or in African American patients is anarea for further study. For the time being,the question has not led to different recom-mendations about testing A1C or to differ-ent interpretations of the clinical meaningof given levels of A1C 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 for A1C.

2. Glycemic goals in adultsRecommendationsc Lowering A1C to below or around 7%has been shown to reducemicrovascular

Table 8dCorrelation 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 16.5These 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 (ref. 67). A calculator for convertingA1C results into eAG, in either mg/dL or mmol/L, isavailable at http://professional.diabetes.org/eAG.


Position Statement

complications of diabetes, and if im-plemented soon after the diagnosis ofdiabetes is associated with long-termreduction in macrovascular disease.Therefore, a reasonable A1C goal formany nonpregnant adults is,7%. (B)

c Providers might reasonably suggest morestringent A1C goals (such as,6.5%) forselected individual patients, if this can beachieved without significant hypogly-cemia or other adverse effects of treat-ment. Appropriate patientsmight includethose with short duration of diabetes,long life expectancy, and no significantCVD. (C)

c Less-stringent A1C goals (such as,8%)may be appropriate for patients with ahistory of severe hypoglycemia, limitedlife expectancy, advanced microvascularor macrovascular complications, exten-sive comorbid conditions, and those withlongstanding diabetes in whom thegeneral goal is difficult to attain despiteDSME, appropriate glucose monitoring,and effective doses of multiple glucose-lowering agents including insulin. (B)

Hyperglycemia defines diabetes, andglycemic control is fundamental to themanagement of diabetes. The DCCT study(61), a prospective RCT of intensive versusstandard glycemic control in patients withrelatively recently diagnosed type 1 diabe-tes, showed definitively that improvedglycemic control is associated with signif-icantly 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 (70,71) demonstrated persis-tence of these microvascular benefits inpreviously intensively treated subjects,even though their glycemic control approx-imated that of previous standard arm sub-jects during follow-up.

The Kumamoto Study (72) and U.K.Prospective Diabetes Study (UKPDS)(73,74) confirmed that intensive glycemiccontrol was associated with significantlydecreased rates of microvascular and neu-ropathic complications in patients withtype 2 diabetes. Long-term follow-up ofthe UKPDS cohorts showed persistence ofthe effect of early glycemic control onmost microvascular complications (75).

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 bene-fit, although more modest, on onset or

progression of microvascular complica-tions. The Veterans Affairs Diabetes Trial(VADT) showed significant reductions inalbuminuria with intensive (achieved me-dian A1C 6.9%) compared with standardglycemic control but no difference in reti-nopathy and neuropathy (76,77). The Ac-tion in Diabetes and Vascular Disease:Preterax and Diamicron Modified ReleaseControlled Evaluation (ADVANCE) studyof intensive versus standard glycemic con-trol in type 2 diabetes found a statisticallysignificant reduction in albuminuria, butnot neuropathy or retinopathy, with anA1C target of ,6.5% (achieved medianA1C 6.3%) compared with standard ther-apy achieving a median A1C of 7.0%(78). Recent analyses from the Actionto Control Cardiovascular Risk in Diabe-tes (ACCORD) trial have shown lowerrates of onset or progression of early-stage microvascular complications inthe intensive glycemic control arm com-pared with the standard arm (79,80).

Epidemiological analyses of the DCCTand UKPDS (61,62) demonstrate a curvi-linear relationship between A1C and mi-crovascular complications. Such analysessuggest that, on a population level, thegreatest number of complications will beaverted by taking patients from very poorcontrol to fair or good control. These anal-yses also suggest that further lowering ofA1C from7 to 6% is associatedwith furtherreduction in the risk ofmicrovascular com-plications, albeit the absolute risk reduc-tions become much smaller. Given thesubstantially increased risk of hypoglyce-mia (particularly in those with type 1 dia-betes, but also in the recent type 2 trials),the concerning mortality findings in theACCORD trial (81), and the relativelymuch greater effort required to achievenear-normoglycemia, the risks of lower gly-cemic targets may outweigh the potentialbenefits on microvascular complicationson a population level. However, selectedindividual patients, especially those withlittle comorbidity and long life expectancy(who may reap the benefits of further low-ering of glycemia below 7%)may, based onprovider judgment andpatient preferences,adopt more-intensive glycemic targets (forexample, an A1C target ,6.5%) as longas significant hypoglycemia does notbecome a barrier.

CVD, a more common cause of deathin populations with diabetes than micro-vascular complications, is less clearly im-pacted by levels of hyperglycemia orintensity of glycemic control. In the DCCT,there was a trend toward lower risk of CVD

events with intensive control, and in 9-yearpost-DCCT follow-up of the EDIC cohortparticipants previously randomized to theintensive arm had a significant 42% re-duction in CVD outcomes and a significant57% reduction in the risk of nonfatalmyocardial infarction (MI), stroke, orCVD death compared with those previ-ously in the standard arm (82). The benefitof intensive glycemic control in this type 1cohort has recently been shown to persistfor several decades (83).

In type 2 diabetes, there is evidencethat more-intensive treatment of glycemiain newly diagnosed patients may reducelong-term CVD rates. During the UKPDStrial, there was a 16% reduction in cardio-vascular events (combined fatal or nonfatalMI and sudden death) in the intensiveglycemic control arm, although this differ-ence was not statistically significant (P 50.052), and therewas no suggestion of ben-efit on other CVD outcomes such as stroke.However, after 10 years of follow-up, thoseoriginally randomized to intensive glyce-mic control had significant long-term re-ductions in MI (15% with sulfonylurea orinsulin as initial pharmacotherapy, 33%with metformin as initial pharmacother-apy) and in all-cause mortality (13 and27%, respectively) (75).

However, results of threemore-recentlarge trials (ACCORD, ADVANCE, andVADT) suggest no significant reductionin CVD outcomes with intensive glycemiccontrol in these populations, who hadmoreadvanced diabetes than UKPDS partici-pants. All three of these trials were conduc-ted in participants with more-long-standingdiabetes (mean duration 8–11 years) andeither known CVD or multiple cardiovas-cular risk factors. Details of these threestudies are reviewed extensively in anADA position statement (84).

The ACCORD study enrolled partic-ipants with either known CVD or two ormore major CV risk factors and random-ized them to intensive glycemic control(goal A1C ,6%) or standard glycemiccontrol (goal A1C 7–8%). The glycemiccontrol arm of ACCORD was halted earlydue to the finding of an increased rate ofmortality in the intensive arm comparedwith the standard arm (1.41 vs. 1.14%peryear; HR 1.22, 95% CI 1.01–1.46), with asimilar increase in cardiovascular deaths.This increase in mortality in the intensiveglycemic control arm was seen in all pre-specified patient subgroups. The primaryoutcome of ACCORD (MI, stroke, or car-diovascular death) was nonsignificantlylower in the intensive glycemic control


Position Statement

group, due to a reduction in nonfatal MI,both when the glycemic control interven-tion was halted (81) and at completion ofthe planned follow-up (85).

Exploratory analyses of the mortalityfindings of ACCORD (evaluating variablesincluding weight gain, use of any specificdrug or drug combination, and hypogly-cemia) were reportedly unable to identify aclear explanation for the excess mortality inthe intensive arm (81). The ACCORD in-vestigators subsequently published addi-tional epidemiologic analyses showing noincrease in mortality in either the intensivearm participants who achieved A1C levels,7% or those who lowered their A1Cquickly after trial enrollment. In fact, al-though there was no A1C level at whichintensive arm participants had significantlylower mortality than standard arm partici-pants, the highest risk for mortality wasobserved in intensive arm participantswith the highest A1C levels (86).

The role of hypoglycemia in the ex-cess mortality findings was also complex.Severe hypoglycemia was significantlymore likely in participants randomizedto the intensive glycemic control arm.However, excess mortality in the intensiveversus standard arms was only significantfor participants with no severe hypoglyce-mia, and not for those with one or moreepisodes. Severe hypoglycemia was associ-ated with excess mortality in either arm,but the association was stronger in thoserandomized to the standard glycemic con-trol arm (87). Unlike the case with theDCCT, where lower achieved A1C levelswere related to significantly increased ratesof severe hypoglycemia, in ACCORD every1% decline in A1C from baseline to 4months into the trial was associatedwith a significant decrease in the rate ofsevere hypoglycemia in both arms (86).

The primary outcome of ADVANCEwas a combination of microvascular events(nephropathy and retinopathy) and majoradverse cardiovascular events (MI, stroke,and cardiovascular death). Intensive glyce-mic control (to a goal A1C,6.5% vs. treat-ment to local standards) significantlyreduced the primary end point. However,this was due to a significant reduction inthe microvascular outcome, primarily de-velopment of macroalbuminuria, with nosignificant reduction in the macrovascularoutcome.Therewas nodifference in overallor cardiovascular mortality between the in-tensive compared with the standard glyce-mic control arms (78).

VADT randomized participants withtype 2 diabetes who were uncontrolled on

insulin or maximal-dose oral agents(median entry A1C 9.4%) to a strategyof intensive glycemic control (goal A1C,6.0%) or standard glycemic control,with a planned A1C separation of at least1.5%. The primary outcome of VADTwas a composite of CVD events. The cu-mulative primary outcome was nonsig-nificantly lower in the intensive arm(76). An ancillary study of VADT demon-strated that intensive glycemic controlwas quite effective in reducing CVDevents in individuals with less atheroscle-rosis at baseline (assessed by coronarycalcium) but not in those with more ex-tensive baseline atherosclerosis (88).

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-analysisof the latter three trials suggests thatglucose lowering has a modest (9%) butstatistically significant reduction in majorCVD outcomes, primarily nonfatal MI,with no significant effect on mortality.However, heterogeneity of the mortalityeffects across studies was noted, precludingfirm summary measures of the mortalityeffects. A prespecified subgroup analysissuggested that major CVD outcome reduc-tion occurred in patients without knownCVD at baseline (HR 0.84, 95% CI 0.74–0.94) (89). Conversely, the mortality find-ings in ACCORD and subgroup analyses ofVADT suggest that the potential risks ofvery intensive glycemic control may out-weigh its benefits in some patients, such

as those with very long duration of diabe-tes, known history of severe hypoglycemia,advanced atherosclerosis, and advancedage/ frailty. Certainly, providers should bevigilant in preventing severe hypoglycemiain patients with advanced disease andshould not aggressively attempt to achievenear-normal A1C levels in patients inwhom such a target cannot be reasonablyeasily and safely achieved. Severe or fre-quent hypoglycemia is an absolute indica-tion for the modification of treatmentregimens, including setting higher glyce-mic goals. Many factors, including patientpreferences, should be taken into accountwhen developing a patient’s individualizedgoals (79).

Recommended glycemic goals formany nonpregnant adults are shown inTable 9. The recommendations are basedon those for A1C values, with listed bloodglucose levels that appear to correlate withachievement of an A1C of,7%. The issueof pre- versus postprandial SMBG targets iscomplex (90). Elevated postchallenge (2-hOGTT) glucose values have been associatedwith increased cardiovascular risk indepen-dent of FPG in some epidemiological stud-ies. In diabetic subjects, some surrogatemeasures of vascular pathology, such as en-dothelial dysfunction, are negatively af-fected by postprandial hyperglycemia(91). It is clear that postprandial hypergly-cemia, like preprandial hyperglycemia,contributes to elevated A1C levels, withits relative contribution being higher atA1C levels that are closer to 7%. However,outcome studies have clearly shown A1Cto be the primary predictor of complica-tions, and landmark glycemic control trials

Table 9dSummary of glycemic recommendations for many nonpregnant adultswith diabetes

A1C ,7.0%*Preprandial capillary plasma glucose 70–130 mg/dL* (3.9–7.2 mmol/L)

Peak postprandial capillary plasma glucose†c Goals should be individualized based on*

○ duration of diabetes○ age/life expectancy○ comorbid conditions○ known CVD or advanced microvascularcomplications

○ hypoglycemia unawareness○ individual patient considerations

c More- or less-stringent glycemic goals may beappropriate for individual patients

c Postprandial glucosemay be targeted if A1C goals arenot met despite reaching preprandial glucose goals

,180 mg/dL* (,10.0 mmol/L)

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


Position Statement

such as the DCCT and UKPDS relied over-whelmingly on preprandial SMBG. Addi-tionally, an RCT in patients with knownCVD found no CVD benefit of insulin regi-mens targeting postprandial glucose com-pared with those targeting preprandialglucose (92). For individualswhohave pre-meal glucose values within target but whohave A1C values above target, monitoringpostprandial plasma glucose (PPG) 1–2 hafter the start of the meal and treatmentaimed at reducing PPG values to ,180mg/dLmay help lower A1C and is a reason-able recommendation for postprandial test-ing and targets. Glycemic goals for childrenare provided in section VII.A.1.a. GlycemicControl.

As regards goals for glycemic controlfor women with GDM, recommendationsfrom the Fifth International Workshop-Conference on Gestational Diabetes (93)are to target maternal capillary glucoseconcentrations of:

c preprandial:#95mg/dL (5.3 mmol/L),and either:

c 1-h postmeal:#140mg/dL (7.8mmol/L)or

c 2-h postmeal:#120mg/dL (6.7mmol/L)

For women with preexisting type 1 ortype 2 diabetes who become pregnant, arecent consensus statement (94) recom-mended the following as optimal glycemicgoals, if they can be achieved without ex-cessive hypoglycemia:

c premeal, bedtime, and overnight glucose60–99 mg/dL (3.3–5.4 mmol/L)

c peak postprandial glucose 100–129mg/dL (5.4–7.1 mmol/L)

c A1C ,6.0%

D. Pharmacologic and overallapproaches to treatment1. Therapy for type 1 diabetes. TheDCCT clearly showed that intensive in-sulin therapy (three or more injections perday of insulin, continuous subcutaneousinsulin infusion [CSII], or insulin pumptherapy) was a key part of improvedglycemia and better outcomes (61,82). Atthe time of the study, therapy was carriedoutwith short- and intermediate-actinghu-man insulins. Despite better microvascularoutcomes, intensive insulin therapywas as-sociated with a high rate in severe hypogly-cemia (62 episodes per 100 patient-years oftherapy). Since the time of the DCCT, anumber of rapid-acting and long-actinginsulin analogs have been developed.These analogs are associated with less

hypoglycemia with equal A1C-loweringin type 1 diabetes (95,96).

Therefore, recommended therapy fortype 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 prandial insu-lin to carbohydrate intake, premeal bloodglucose, and anticipated activity; and 3)for many patients (especially if hypogly-cemia is a problem), use of insulin ana-logs. There are excellent reviews availablethat guide the initiation and managementof insulin therapy to achieve desired gly-cemic goals (3,95,97).

Because of the increased frequency ofother autoimmune diseases in type 1 di-abetes, 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 frequency areunclear.

2. Therapy for type 2 diabetes

Recommendationsc At the time of type 2 diabetes diagnosis,initiate metformin therapy along withlifestyle interventions, unless metfor-min is contraindicated. (A)

c In newly diagnosed type 2 diabetic pa-tients with markedly symptomatic and/or elevated blood glucose levels or A1C,consider insulin therapy, with or with-out additional agents, from the outset. (E)

c If noninsulin monotherapy at maximaltolerated dose does not achieve or main-tain the A1C target over 3–6 months,add a second oral agent, a GLP-1 receptoragonist, or insulin. (E)

Prior expert consensus statementshave suggested approaches to manage-ment of hyperglycemia in individualswith type 2 diabetes (98). Highlights in-clude intervention at the time of diagnosiswith metformin in combination with life-style changes (MNT and exercise) and con-tinuing timely augmentation of therapywith additional agents (including early ini-tiation of insulin therapy) as a means ofachieving and maintaining recommendedlevels of glycemic control (i.e., A1C ,7%for most patients). As A1C targets are notachieved, treatment intensification is basedon the addition of another agent from adifferent class. Meta-analyses (99) suggestthat overall, each new class of noninsulinagents added to initial therapy lowers A1Caround 0.9–1.1%. The overall objective is

to safely achieve and maintain glycemiccontrol and to change interventions whentherapeutic goals are not being met.

ADA and EASD have partnered onnew guidance for individualization of useof medication classes and combinationsin patients with type 2 diabetes. Theseguidelines, to be published in early 2012,will be less prescriptive than prior algo-rithms, and will discuss advantages anddisadvantages of the available medicationclasses as well as considerations for theiruse. For information about currently ap-proved classes of medications for treat-ing hyperglycemia in type 2 diabetes, seeTable 10.

E. Medical nutrition therapy (MNT)General recommendationsc Individuals who have prediabetes ordiabetes should receive individualizedMNT as needed to achieve treatmentgoals, preferably provided by a regis-tered dietitian familiar with the compo-nents of diabetes MNT. (A)

c Because MNT can result in cost-savingsand improvedoutcomes (B),MNTshouldbe adequately covered by insurance andother payers. (E)

Energy balance, overweight, and obesityc Weight loss is recommended for alloverweight or obese individuals whohave or are at risk for diabetes. (A)

c 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)

c 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)

c Physical activity and behavior modifi-cation are important components ofweight loss programs and aremost helpfulin maintenance of weight loss. (B)

Recommendations for primary preventionof diabetesc Among individuals at high risk for de-veloping type 2 diabetes, structuredprograms that emphasize lifestyle changesthat include moderate weight loss (7%body weight) and regular physical ac-tivity (150 min/week), with dietarystrategies including reduced calories andreduced intake of dietary fat, can reducethe risk for developing diabetes and aretherefore recommended. (A)

c Individuals at risk for type 2 diabetesshould be encouraged to achieve theU.S. Department of Agriculture (USDA)recommendation for dietary fiber (14 g


Position Statement

Table

10d

Noninsulin

therap

iesforhyperglycemia

intype

2diab

etes:properties

ofselected

glucose-loweringdrugsthat

may

guideindividu

alizationof

therap

y

Class

Com

pound

(s)

Mechanism

Action(s)

Adv

antages

Disadvantages

Cost

Biguanides

Metform

inActivates

AMP-kinase

cHepaticglucose

prod

uctio

n↓

cIntestinalglucose

absorption

↓cInsulin

action

↑

cNoweightgain

cNohypoglycemia

cReduction

incardiovascular

eventsand

mortality

(UKPD

Sf/u)

cGastrointestinalsideeffects

(diarrhea,abdom

inal

cram

ping)

cLacticacidosis(rare)

cVitam

inB 1

2deficiency

cCon

traind

ications:reduced

kidneyfunction

Low

Sulfo

nylureas

(2nd

generation)

cGlib

enclam

ide/

Glybu

ride

cGlip

izide

cGliclazide

cGlim

epiride

ClosesKATP

channelson

b-cell

plasmamem

branes

c↑Insulin

secretion

cGenerallywell

tolerated

cReduction

incardiovascular

eventsand

mortality

(UKPD

Sf/u)

cRelativelyglucose-independent

stim

ulationof

insulin

secretion:

Hyp

oglycemia,including

episod

esnecessitatingho

spital

admission

andcausingdeath

cWeightgain

cMay

blunt

myocardialischemic

precon

ditio

ning

cLo

w“durability”

Low

Meglitinides

cRepaglin

ide

cNateglin

ide

ClosesKATP

channelson

b-cell

plasmamem

branes

Insulin

secretion↑

Accentuated

effects

arou

ndmeal

ingestion

cHyp

oglycemia,w

eigh

tgain,

cMay

blunt

myocardialischemic

precon

ditio

ning

cDosingfrequency

Medium

Thiazolid

inediones

(Glitazon

es)

cPioglitazon

eActivates

thenu

clear

transcription

factor

PPAR-g

cPeriph

eralinsulin

sensitivity

↑cNohypoglycemia

cHDLcholesterol↑

cTriglycerides

↓

cWeightgain

cEdema

cHeartfailu

re

cBo

nefractures

High

cRosiglitazon

eAsabove

Asabove

Nohypoglycemia

cLD

Lcholesterol↑

cWeightgain

cEdema

cHeartfailu

re

cBo

nefractures

cIncreasedcardiovascularevents

(mixed

evidence)

cFD

Awarnings

oncardiovascular

safety

cCon

traind

icated

inpatientswith

heartdisease

High

a-Glucosidase

inhibitors

cAcarbose

cMiglitol

Inhibits

intestinal

a-glucosidase

Intestinalcarboh

ydrate

digestion(and

,consecutiv

ely,

absorption

)slow

ed

cNon

system

icmedication

cPo

stprandial

glucose

↓

cGastrointestinalsideeffects(gas,

flatulence,d

iarrhea)

cDosingfrequency

Medium


Position Statement

fiber/1,000 kcal) and foods containingwhole grains (one-half of grain intake).(B)

c Individuals at risk for type 2 diabetesshould be encouraged to limit their in-take of sugar-sweetened beverages. (B)

Recommendations for management ofdiabetesMacronutrients in diabetes managementc The mix of carbohydrate, protein, andfat may be adjusted to meet the meta-bolic goals and individual preferencesof the person with diabetes. (C)

c Monitoring carbohydrate, whether bycarbohydrate counting, choices, or ex-perience-based estimation, remains a keystrategy in achieving glycemic control. (B)

c Saturated fat intake should be ,7% oftotal calories. (B)

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

Other nutrition recommendationsc If adults with diabetes choose to usealcohol, they should limit intake to amoderate amount (one drink per day orless for adult women and two drinks perday or less for adult men) and shouldtake extra precautions to prevent hypo-glycemia. (E)

c Routine supplementation with anti-oxidants, 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)

c It is recommended that individualizedmeal planning include optimization offood choices to meet recommendeddaily allowance (RDA)/dietary referenceintake (DRI) for all micronutrients. (E)

MNT is an integral component ofdiabetes prevention, management, andself-management education. In additionto its role in preventing and controllingdiabetes, ADA recognizes the importanceof nutrition as an essential component ofan overall 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 updatedin 2008 (100). Achieving nutrition-relatedgoals requires a coordinated team effortthat includes the active involvement ofthe person with prediabetes or diabetes.Because of the complexity of nutritionT

able

10dCon

tinu

ed

Class

Com

poun

d(s)

Mechanism

Action(s)

Advantages

Disadvantages

Cost

GLP

-1receptor

agon

ists

(incretin

mim

etics)

cExenatid

e

cLiraglutide

Activates

GLP

-1receptors(b-cells/

endocrine

pancreas;

brain/auton

omou

snervou

ssystem

)

cInsulin

secretion↑

(glucose-dependent)

cGlucagonsecretion↓

(glucose-dependent)

cSlow

sgastricem

ptying

cSatiety

↑

cWeigh

treductio

n

cPo

tentialfor

improvedb-cell

mass/function

cGastrointestinalsideeffects(nausea,

vomiting,diarrhea)

cCases

ofacutepancreatitisob

served

cC-cellhyperplasia/m

edullary

thyroidtumorsinanimals(liraglutide)

cInjectable

cLo

ng-term

safety

unkn

own

High

DPP

-4inhibitors

(incretin

enhancers)

cSitagliptin

cVild

aglip

tin

cSaxagliptin

cLinaglip

tin

InhibitsDPP

-4activity,

prolon

gssurvivalof

endogenou

slyreleased

incretin

horm

ones

cActiveGLP

-1concentration↑

cActiveGIP

concentration↑

cInsulin

secretion↑

cGlucagonsecretion↓

cNohy

poglycem

ia

cWeigh

t“neutrality”

cOccasionalreportsof

urticaria/

angioedem

a

cCases

ofpancreatitisob

served

cLo

ng-term

safety

unkn

own

High

Bileacid

sequ

estrants

Colesevelam

Binds

bileacids/

cholesterol

cUnk

nown

cNohy

poglycem

ia

cLD

Lcholesterol↓

cCon

stipation

cTriglycerides

↑cMay

interferewithabsorption

ofother

medications

High

Dop

amine-2

agon

ists

Brom

ocriptine

Activates

dopaminergic

receptors

cAltershy

pothalam

icregu

lation

ofmetabolism

cInsulin

sensitivity

↑

Nohypoglycemia

cDizziness/syncope

cNausea

cFatig

ue

cRhinitis

cLo

ng-term

safety

unkn

own

Medium

Adaptedwith

perm

ission

from

Silvio

Inzucchi,YaleUniversity

.PPA

R,p

eroxisom

eproliferator–activatedreceptor.


Position Statement

issues, it is recommended that a registereddietitianwho is knowledgeable and skilledin implementing nutrition therapy into di-abetes management and education be theteam member who provides 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 studieshave demonstrated sustained improve-ments in A1C at 12 months and longerwhen an registered dietitian providedfollow-up visits ranging from monthly tothree sessions per year (101–108). Studiesin nondiabetic suggest that MNT reducesLDL cholesterol by 15–25 mg/dL up to16% (109) and support a role for life-style modification in treating hypertension(109,110).

While the importance of weight lossfor overweight and obese individuals iswell documented, an optimal macronu-trient distribution and dietary pattern ofweight loss diets has not been established.A systematic review of 80 weight lossstudies of $1 year duration demonstratedthatmoderate weight loss achieved throughdiet alone, diet and exercise, and meal re-placements can be achieved and main-tained (4.8–8% weight loss at 12 months)(111). Both low-fat low-carbohydrate andMediterranean style eating patterns havebeen shown to promote weight loss withsimilar results after 1 to 2 years of follow-up(112–115). A meta-analysis showed thatat 6 months, low-carbohydrate diets wereassociated with greater improvements intriglyceride and HDL cholesterol concen-trations than low-fat diets; however, LDLcholesterol was significantly higher on thelow-carbohydrate diets (116).

Because of the effects of obesity oninsulin resistance, weight loss is an impor-tant therapeutic objective for overweight orobese individuals who are at risk for di-abetes (117). The multifactorial intensivelifestyle intervention employed in theDPP, which included reduced intake offat and calories, led toweight loss averaging7% at 6 months and maintenance of5% weight loss at 3 years, associatedwith a 58% reduction in incidence oftype 2 diabetes (20). A RCT looking athigh-risk individuals in Spain showed theMediterranean dietary pattern reduced theincidence of diabetes in the absence ofweight loss by 52% compared with thelow-fat diet control group (118).

Although our society abounds withexamples of high-calorie nutrient-poorfoods, large increases in the consumption

of sugar-sweetened beverages have coin-cided with the epidemics of obesity andtype 2 diabetes. In a meta-analysis of eightprospective cohort studies (N5 310,819), adiet high in consumptionof sugar-sweetenedbeverages was associated with the devel-opment of type 2 diabetes (n 5 15,043).Individuals in the highest versus the low-est quantile of sugar-sweetened beverageintake had a 26% greater risk of develop-ing diabetes (119).

For individuals with type 2 diabetes,studies have demonstrated that moderateweight loss (5% of body weight) is asso-ciated with decreased insulin resistance,improved measures of glycemia and lipe-mia, and reduced blood pressure (120);longer-term studies ($52 weeks) showedmixed effects on A1C in adults with type 2diabetes (121–123), and in some studiesresults were confounded by pharmaco-logic weight loss therapy. Look AHEAD(Action for Health in Diabetes) is a largeclinical trial designed to determine whetherlong-term weight loss will improve glyce-mia and prevent cardiovascular events insubjects with type 2 diabetes. One-year re-sults of the intensive lifestyle interventionin this trial show an average 8.6% weightloss, significant reduction of A1C, and re-duction in several CVD risk factors (124),with benefits sustained at 4 years (125).When completed, the Look AHEAD trialshould provide insight into the effects oflong-termweight loss on important clinicaloutcomes.

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. Thebest mix of carbohydrate, protein, and fatappears to vary depending on individualcircumstances. It must be clearly recog-nized that regardless of the macronutrientmix, total caloric intake must be appropri-ate to weight management goal. Further,individualization of the macronutrientcomposition will depend on the metabolicstatus of the patient (e.g., lipid profile, renalfunction) and/or food preferences. Avariety of dietary meal patterns are likelyeffective in managing diabetes includingMediterranean-style, plant-based (vegan orvegetarian), low-fat and lower-carbohydrateeating patterns (113,126–128).

It should be noted that the RDA fordigestible carbohydrate is 130 g/day andis based on providing adequate glucose asthe required fuel for the central nervoussystem without reliance on glucose pro-duction from ingested protein or fat.

Although brain fuel needs can be met onlower-carbohydrate diets, long-term meta-bolic effects of very-low-carbohydratediets are unclear, and such diets eliminatemany foods that are important sources ofenergy, fiber, vitamins, and minerals andthat are important in dietary palatability(129).

Saturated and trans fatty acids are theprincipal dietary determinants of plasmaLDL cholesterol. There is a lack of evidenceon the effects of specific fatty acids on peo-ple with diabetes; the recommended goalsare therefore consistent with those for indi-viduals with CVD (109,130).

Reimbursement for MNTMNT, when delivered by a registereddietitian according to nutrition practiceguidelines, is reimbursed as part of theMedicare program as overseen by theCenters for Medicare andMedicaid Serv-ices (CMS) (www.cms.gov).

F. Diabetes self-managementeducation (DSME)Recommendationsc People with diabetes should receiveDSME according to national standardsand diabetes self-management supportwhen their diabetes is diagnosed and asneeded thereafter. (B)

c Effective self-management and qualityof life are the key outcomes of DSMEand should be measured and monitoredas part of care. (C)

c DSME should address psychosocialissues, since emotional well-being isassociated with positive diabetes out-comes. (C)

c Because DSME can result in cost-savingsand improved outcomes (B), DSMEshould be adequately reimbursed bythird-party payers. (E)

DSME is an essential element of di-abetes care (131–136), and nationalstandards for DSME (137) are based onevidence for its benefits. Education helpspeople with diabetes initiate effective self-management and cope with diabetes whenthey are first diagnosed. Ongoing DSMEand diabetes self-management support(DSMS) also help people with diabetesmaintain effective self-managementthroughout a lifetime of diabetes as theyface new challenges and as treatment ad-vances become available. DSME helps pa-tients optimize metabolic control, preventand manage complications, and maximizequality of life in a cost-effective manner(138).


Position Statement

DSME and DSMS are the on-goingprocesses of facilitating the knowledge,skill, and ability necessary for diabetesself-care. This process incorporates theneeds, goals, and life experiences of theperson with diabetes. The overall objec-tives of DSME and DSMS are to supportinformed decision-making, self-care be-haviors, problem-solving, and active col-laboration with the health care team toimprove clinical outcomes, health status,and quality of life in a cost-effective man-ner (137).

Current best practice for DSME is askills-based approach that focuses onhelping those with diabetes make in-formed self-management choices. DSMEhas changed from a didactic approachfocusing on providing information tomore theoretically based empowermentmodels that focus on helping those withdiabetes make informed self-managementdecisions. Care of diabetes has shifted to anapproach that is more patient centered andplaces the person with diabetes and his orher family at the center of the care modelworking in collaboration with health careprofessionals. Patient-centered care is re-spectful of and responsive to individualpatient preferences, needs, and values andensures that patient’s values guide all deci-sion making (139).Evidence for the benefits of DSME. Mul-tiple studies have found that DSME isassociated with improved diabetes knowl-edge and self-care behavior (131), improvedclinical outcomes such as lower A1C(132,133,135,136,140,141), lower self-reported weight (131), improved qualityof life (134,141,142), healthy coping(143), and lower costs (144). Better out-comes were reported for DSME inter-ventions that were longer and includedfollow-up support (DSMS) (131,145–149)(150), that were culturally (151,152) andage appropriate (153,154), that were tai-lored to individual needs and prefer-ences, and that addressed psychosocialissues and incorporated behavioral strat-egies (131,135,155–157). Both individualand group approaches have been foundeffective (158–161). There is growing evi-dence for the role of community healthworkers and peer (162,163) and lay leaders(164) in delivering DSME and support inaddition to the core team (165).

Diabetes education is associated withincreased use of primary and preventiveservices and lower use of acute, inpatienthospital services (144). Patients who par-ticipate in diabetes education are morelikely to follow best practice treatment

recommendations, particularly amongthe Medicare population, and have lowerMedicare and commercial claim costs(166,167).National standards for DSME. Thenational standards for DSME are designedto define quality DSME and to assistdiabetes educators in a variety of settingsto provide evidence-based education(137). The standards, currently being up-dated, are reviewed and updated every5 years by a task force representing keyorganizations involved in the field of di-abetes education and care.Reimbursement for DSME. DSME,when provided by a program that meetsnational standards for DSME and is recog-nized by ADA or other approval bodies, isreimbursed as part of theMedicare programas overseen by the Centers for Medicare andMedicaid Services (CMS) (www.cms.gov).DSME is also covered by most health insur-ance plans.

G. Physical activityRecommendationsc People with diabetes should be advisedto perform at least 150 min/week ofmoderate-intensity aerobic physicalactivity (50–70% of maximum heartrate), spread over at least 3 days perweek with no more than 2 consecutivedays without exercise. (A)

c In the absence of contraindications,people with type 2 diabetes should beencouraged to perform resistance train-ing at least twice per week. (A)

Exercise is an important part of thediabetes management plan. Regular exer-cise has been shown to improve bloodglucose control, reduce cardiovascular riskfactors, contribute to weight loss, andimprove well-being. Furthermore, regularexercise may prevent type 2 diabetes inhigh-risk individuals (20–22). Structuredexercise interventions of at least 8-weekduration have been shown to lower A1Cby an average of 0.66% in people withtype 2 diabetes, even with no significantchange in BMI (168). Higher levels of ex-ercise intensity are associated withgreater improvements in A1C and in fit-ness (169). A joint position statement byADA and the American College of SportsMedicine summarizes the evidence for ben-efits of exercise in people with type 2 diabe-tes (170).Frequency and type of exercise.The U.S. Department of Health and Hu-man Services’ “Physical Activity Guide-lines for Americans” (171) suggests that

adults over age 18 years perform 150 minper week of moderate-intensity or 75 minper week of vigorous aerobic physical activ-ity or an equivalent combination of the two.In addition, the guidelines suggest thatadults also perform muscle-strengtheningactivities that involve all major musclegroups2ormore days perweek. The guide-lines suggest that adults over age 65 years,or those with disabilities, follow the adultguidelines if possible or (if this is not pos-sible) be as physically active as they are able.Studies included in a meta-analysis of theeffects of exercise interventions on glycemiccontrol (168) had a mean number of ses-sions per week of 3.4, with amean durationof 49 min per session. The DPP lifestyle in-tervention, which included 150 min perweek of moderate-intensity exercise, had abeneficial effect on glycemia in those withprediabetes. Therefore, it seems reasonableto recommend that people with diabetes tryto follow the physical activity guidelines forthe general population.

Progressive resistance exercise im-proves insulin sensitivity in older menwith type 2 diabetes to the same or even agreater extent as aerobic exercise (172).Clinical trials have provided strong evi-dence for the A1C lowering value of resis-tance training in older adults with type 2diabetes (173,174), and for an additivebenefit of combined aerobic and resistanceexercise in adults with type 2 diabetes(175,176). In the absence of contraindica-tions, patients with type 2 diabetes shouldbe encouraged to do at least two weeklysessions of resistance exercise (exercisewith free weights or weight machines),with each session consisting of at leastone set of five or more different resistanceexercises involving the large muscle groups(170).Evaluation of the diabetic patient beforerecommending an exercise program.Prior guidelines suggested that beforerecommending a program of physicalactivity, the provider should assess pa-tients with multiple cardiovascular riskfactors for coronary artery disease (CAD).As discussed more fully in section VI.A.5.CHD Screening and Treatment, the area ofscreening asymptomatic diabetic patientsfor CAD remains unclear, and a recent ADAconsensus statement on this issue con-cluded that routine screening is not rec-ommended (177). Providers should useclinical judgment in this area. Certainly,high-risk patients should be encouragedto start with short periods of low-inten-sity exercise and increase the intensityand duration slowly.


Position Statement

Providers should assess patients forconditions that might contraindicate certaintypes of exercise or predispose to injury,such as uncontrolled hypertension, se-vere 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 of nonoptimalglycemic control hyperglycemia. Whenpeople with type 1 diabetes are deprivedof insulin for 12–48 h and are ketotic,exercise can worsen hyperglycemia andketosis (178); therefore, vigorous activityshould be avoided in the presence of ke-tosis. However, it is not necessary topostpone exercise based simply on hy-perglycemia, provided the patient feelswell and urine and/or blood ketones arenegative.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 preexercise glucoselevels are ,100 mg/dL (5.6 mmol/L).Hypoglycemia is rare in diabetic individ-uals who are not treated with insulin orinsulin secretagogues, and no preventivemeasures for hypoglycemia are usuallyadvised 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 (179).

Peripheral neuropathy. Decreased painsensation in the extremities results inincreased risk of skin breakdown andinfection and of Charcot joint destruction.Prior recommendations have advised non–weight-bearing exercise for patients withsevere peripheral neuropathy. However,studies have shown that moderate-intensitywalking may not lead to increased risk offoot ulcers or reulceration in those withperipheral neuropathy (180). All indi-viduals with peripheral neuropathyshould wear proper footwear and exam-ine their feet daily to detect lesions early.Anyone with a foot injury or open soreshould be restricted to non–weight-bearing activities.

Autonomic neuropathy.Autonomic neuropathy can increase therisk of exercise-induced injury or ad-verse event through decreased cardiacresponsiveness to exercise, postural hy-potension, impaired thermoregulation,impaired night vision due to impairedpapillary reaction, and unpredictable car-bohydrate delivery from gastroparesis pre-disposing to hypoglycemia (181).Autonomic neuropathy is also strongly as-sociated with CVD in people with diabetes(182,183). People with diabetic auto-nomic neuropathy should undergo car-diac investigation before beginningphysical activity that is more intensethan that to which they are accustomed.Albuminuria and nephropathy.Physical activity can acutely increase uri-nary protein excretion. However, there isno evidence that vigorous exercise increa-ses the rate of progression of diabetickidney disease, and there is likely no needfor any specific exercise restrictions forpeople with diabetic kidney disease(184).

H. Psychosocial assessment and careRecommendationsc It is reasonable to include assessment ofthe patient’s psychological and socialsituation as an ongoing part of themedical management of diabetes. (E)

c Psychosocial screening and follow-upmay include, but is not limited to, atti-tudes about the illness, expectations formedical management and outcomes,affect/mood, general and diabetes-related quality of life, resources (financial,social, and emotional), and psychiatrichistory. (E)

c Consider screening for psychosocialproblems such as depression anddiabetes-related distress, anxiety, eat-ing disorders, and cognitive impairmentwhen self-management is poor. (C)

Psychological and social problemscan impair the individual’s (185–188) orfamily’s ability to carry out diabetes caretasks and therefore compromise healthstatus. There are opportunities for the cli-nician to assess psychosocial status in atimely and efficient manner so that re-ferral for appropriate services can beaccomplished. A systematic review andmeta-analysis showed that psychosocialinterventions modestly but significantlyimproved A1C (standardized meandifference 20.29%) and mental healthoutcomes. However, a limited associationbetween the effects on A1C and mental

health, and no intervention characteris-tics predicted benefit on both outcomes,was shown (189).

Key opportunities for screening ofpsychosocial status occur at diagnosis,during regularly scheduled managementvisits, during hospitalizations, at discoveryof complications, or when problems withglucose control, quality of life, or adherenceare identified. Patients are likely to exhibitpsychological vulnerability at diagnosisand when their medical status changes,e.g., the end of the honeymoon period,when the need for intensified treatment isevident, and when complications are dis-covered (187).

Issuesknownto impact self-managementand health outcomes include but are notlimited to attitudes about the illness,expectations for medical managementand outcomes, affect/mood, general anddiabetes-related quality of life, diabetes-related distress (190,191), resources (fi-nancial, social, and emotional) (192), andpsychiatric history (193–195). Screeningtools are available for a number of theseareas (156). Indications for referral to amental health specialist familiar with diabe-tes management may include gross non-compliance with medical regimen (by selfor others) (195), depression with the pos-sibility of self-harm, debilitating anxiety(alone or with depression), indications ofan eating disorder (196), or cognitive func-tioning that significantly impairs judgment.It is preferable to incorporate psychologicalassessment and treatment into routine carerather than waiting for identification of aspecific problem or deterioration in psy-chological status (156). Although the cli-nician may not feel qualified to treatpsychological problems, utilizing thepatient-provider relationship as a foun-dation for further treatment can increasethe likelihood that the patient will acceptreferral for other services. It is importantto establish that emotional well-being ispart of 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 9). Rethinking the treatmentregimenmay require assessment of barriersincluding income, health literacy, diabetesdistress, depression, and competing de-mands, including those related to familyresponsibilities and dynamics. Other strat-egies may include culturally appropriateand enhanced DSME, co-managementwith a diabetes team, referral to a medical


Position Statement

social worker for assistance with insurancecoverage, or change in pharmacologicaltherapy. Initiation of or increase in SMBG,utilization of continuous glucose monitor-ing, frequent contact with the patient, orreferral to a mental health professional orphysician with special expertise in diabetesmay be useful. Providing patients with analgorithm for self-titration of insulin dosesbased on SMBG results may be helpful fortype 2 patients who take insulin (197).

J. Intercurrent illnessThe stress of illness, trauma, and/or surgeryfrequently aggravates glycemic control andmay precipitate diabetic ketoacidosis(DKA) or nonketotic hyperosmolar statedlife-threatening conditions that requireimmediate medical care to prevent com-plications and death. Any condition lead-ing to deterioration in glycemic controlnecessitates more frequent monitoringof blood glucose and (in ketosis-pronepatients) urine or blood ketones. Markedhyperglycemia requires temporary ad-justment of the treatment program and,if accompanied by ketosis, vomiting, oralteration in level of consciousness, im-mediate interaction with the diabetescare team. The patient treated with non-insulin therapies or MNT alone may tem-porarily require insulin. Adequate fluidand caloric intake must be assured. In-fection or dehydration are more likely tonecessitate hospitalization of the personwith diabetes than the person withoutdiabetes.

The hospitalized patient should betreated by a physician with expertise inthe management of diabetes. For furtherinformation on management of patientswith hyperglycemia in the hospital, seesection IX.A. Diabetes Care in the Hospital.For further information on management ofDKA or nonketotic hyperosmolar state,refer to the ADA consensus statement onhyperglycemic crises (198).

K. HypoglycemiaRecommendationsc Glucose (15–20 g) is the preferredtreatment 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 ameal orsnack to prevent recurrence of hypo-glycemia. (E)

c Glucagon should be prescribed for allindividuals at significant risk of severehypoglycemia, and caregivers or familymembers of these individuals instructedin its administration. Glucagon admin-istration is not limited to health careprofessionals. (E)

c 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 risk offuture episodes. (B)

Hypoglycemia is the leading limitingfactor in the glycemic management of type1 and insulin-treated type 2 diabetes (199).Mild hypoglycemiamay be inconvenient orfrightening to patients with diabetes, andmore severe hypoglycemia can cause acuteharm to the person with diabetes or others,if it causes falls, motor vehicle accidents, orother injury. A large cohort study suggestedthat among older adults with type 2diabetes, a history of severe hypoglyce-mia was associated with greater risk ofdementia (200). Conversely, evidencefrom the DCCT/EDIC study, which in-volved younger type 1 patients, suggestedno association of frequency of severe hypo-glycemia with cognitive decline (201).Treatment of hypoglycemia (plasmaglucose,70 mg/dL) requires ingestion of glucose-or carbohydrate-containing foods. Theacute glycemic response correlates betterwith the glucose content than with the car-bohydrate content of the food. Althoughpure glucose is the preferred treatment,any form of carbohydrate that contains glu-cosewill raise blood glucose. Added fatmayretard and then prolong the acute glycemicresponse. Ongoing activity of insulin or in-sulin secretagogues may lead to recurrenceof hypoglycemia unless further food is in-gested after recovery.

Severe hypoglycemia (where the in-dividual requires the assistance of anotherperson and cannot be treated with oralcarbohydrate due to confusion or un-consciousness) should be treated usingemergency 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 instruc-ted in use of such kits. An individual doesnot need to be a health care professional tosafely administer glucagon. Care should be

taken to ensure that unexpired glucagonkits are available.

Prevention of hypoglycemia is a crit-ical component of diabetes management.Patients should understand situationsthat increase their risk of hypoglycemia,such as when fasting for tests or proce-dures, during or after intense exercise, andduring sleep; and that increase the risk ofharm to self or others from hypoglycemia,such as with driving. Teaching people withdiabetes to balance insulin use, carbohy-drate intake, and exercise is a necessary butnot always sufficient strategy for preven-tion. In type 1 diabetes and severelyinsulin-deficient type 2 diabetes, the syn-drome of hypoglycemia unawareness, orhypoglycemia-associated autonomic fail-ure, can severely compromise stringentdiabetes control and quality of life. Thedeficient counter-regulatory hormone re-lease and autonomic responses in thissyndrome are both risk factors for, andcaused by, hypoglycemia. A corollary tothis “vicious cycle” is that several weeks ofavoidance of hypoglycemia has beendemonstrated to improve counterregula-tion and awareness to some extent inmany patients (202). Hence, patients withone or more episodes of severe hypoglyce-mia may benefit from at least short-term re-laxation of glycemic targets.

L. Bariatric surgeryRecommendationsc Bariatric surgery may be considered foradults with BMI.35 kg/m2 and type 2diabetes, especially if the diabetes orassociated comorbidities are difficult tocontrol with lifestyle and pharmaco-logic therapy. (B)

c Patients with type 2 diabetes who haveundergone bariatric surgery need life-long lifestyle support and medical moni-toring. (B)

c Although small trials have shown gly-cemic benefit of bariatric surgery inpatients with type 2 diabetes and BMIof 30–35 kg/m2, there is currently in-sufficient evidence to generally rec-ommend surgery in patients with BMI,35 kg/m2 outside of a research pro-tocol. (E)

c The long-termbenefits, cost-effectiveness,and risks of bariatric surgery in indi-viduals with type 2 diabetes should bestudied in well-designed controlledtrials with optimalmedical and lifestyletherapy as the comparator. (E)

Gastric reduction surgery, either gas-tric banding or procedures that involve


Position Statement

bypassing, transposing, or resecting sec-tions of the small intestine, when part of acomprehensive team approach, can be aneffective weight loss treatment for severeobesity, and national guidelines supportits consideration for people with type 2diabetes who have BMI.35 kg/m2. Bariat-ric surgery has been shown to lead to near-or complete normalization of glycemia in;55–95% of patients with type 2 diabetes,depending on the surgical procedure. Ameta-analysis of studies of bariatric surgeryinvolving 3,188 patients with diabetes re-ported that 78% had remission of diabe-tes (normalization of blood glucose levelsin the absence of medications), and thatthe remission rates were sustained instudies that had follow-up exceeding 2years (203). Remission rates tend to belower with procedures that only constrictthe stomach and higher with those thatbypass portions of the small intestine.Additionally, there is a suggestion that in-testinal bypass procedures may have gly-cemic effects that are independent of theireffects on weight, perhaps involving theincretin axis.

One RCT compared adjustable gastricbanding to “best available” medical andlifestyle therapy in subjects with type 2diabetes diagnosed less than 2 years be-fore randomization and with BMI 30–40kg/m2 (204). In this trial, 73% of surgi-cally treated patients achieved “remis-sion” of their diabetes, compared with13% of those treated medically. The lattergroup lost only 1.7% of body weight, sug-gesting that their therapy was not opti-mal. Overall the trial had 60 subjects,and only 13 had a BMI,35 kg/m2, mak-ing it difficult to generalize these resultswidely to diabetic patients who are lessseverely obese or with longer durationof diabetes. In a more recent study involv-ing 110 patients with type 2 diabetesand a mean BMI of 47 kg/m2, Roux-en-Ygastric bypass resulted in a mean loss ofexcess weight of 63% at 1 year and 84% at2 years (205).

Bariatric surgery is costly in the shortterm and has some risks. Rates of mor-bidity andmortality directly related to thesurgery have been reduced considerablyin recent years, with 30-day mortality ratesnow 0.28%, similar to those of laparo-scopic cholecystectomy (206). Longer-term concerns include vitamin andmineraldeficiencies, osteoporosis, and rare but of-ten severe hypoglycemia from insulin hy-persecretion. Cohort studies attempting tomatch subjects suggest that the proceduremay reduce longer-term mortality rates

(207). Recent retrospective analyses andmodeling studies suggest that these proce-dures may be cost-effective, when one con-siders reduction in subsequent health carecosts (208–210).

Some caution about the benefits ofbariatric surgery might come from recentstudies. A propensity score–adjustedanalyses of older severely obese patientswith high baseline mortality in VeteransAffairs Medical Centers found that the useof bariatric surgery was not associatedwith decreased mortality compared withusual care during a mean 6.7 years offollow-up (211). A study that followed pa-tients who had undergone laparoscopicadjustable gastric banding (LAGB) for 12years found that 60% were satisfied withthe procedure. Nearly one of three pa-tients experienced band erosion, and al-most half had required removal of theirbands. The authors’ conclusion was that,“LAGB appears to result in relatively poorlong-term outcomes” (212). Studies of themechanisms of glycemic improvementand long-term benefits and risks of bariat-ric surgery in individuals with type 2 di-abetes, especially those who are notseverely obese, will require well-designedclinical trials, with optimal medical andlifestyle therapy of diabetes and cardiovas-cular risk factors as the comparator.

M. ImmunizationRecommendationsc Annually provide an influenza vaccineto all diabetic patients $6 months ofage. (C)

c Administer pneumococcal polysaccha-ride vaccine to all diabetic patients $2years of age. A one-time revaccination isrecommended for individuals.64 yearsof age previously immunized whenthey were ,65 years of age if the vac-cine was administered .5 years ago.Other indications for repeat vaccina-tion include nephrotic syndrome,chronic renal disease, and other immu-nocompromised states, such as aftertransplantation. (C)

c Administer hepatitis B vaccination toadults with diabetes as per Centers forDisease Control and Prevention (CDC)recommendations. (C)

Influenza and pneumonia are com-mon, preventable infectious diseases asso-ciated with highmortality andmorbidity inthe elderly and in people with chronicdiseases. Though there are limited studiesreporting the morbidity and mortality ofinfluenza and pneumococcal pneumonia

specifically in people with diabetes, obser-vational studies of patients with a variety ofchronic illnesses, including diabetes, showthat these conditions are associated with anincrease in hospitalizations for influenzaand its complications. People with diabetesmay be at increased risk of the bacteremicform of pneumococcal infection andhave been reported to have a high riskof nosocomial bacteremia, which has amortality rate as high as 50% (213).

Safe and effective vaccines are avail-able that can greatly reduce the risk ofserious complications from these diseases(214,215). In a case-control series, influ-enza vaccine was shown to reduce diabe-tes-related hospital admission by as muchas 79% during flu epidemics (214). 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 pneumococcalvaccines for all individuals with diabetes(http://www.cdc.gov/vaccines/recs/).

At the time these standards went topress, the CDC was considering recom-mendations to immunize all or some adultswith diabetes for hepatitis B. ADA awaitsthe final recommendations and will sup-port them when they are released in 2012.

VI. PREVENTION ANDMANAGEMENT OF DIABETESCOMPLICATIONS

A. CVDCVD is the major cause of morbidity andmortality for individuals with diabetesand 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 (216,217). There isevidence that measures of 10-year coro-nary heart disease (CHD) risk among U.S.adults with diabetes have improved sig-nificantly over the past decade (218).

1. Hypertension/blood pressure controlRecommendationsScreening and diagnosisc Blood pressure should be measuredat every routine diabetes visit. Patients


Position Statement

found to have systolic blood pressure(SBP) $ 130mmHg or diastolic bloodpressure (DBP) $80 mmHg shouldhave blood pressure confirmed on aseparate day. Repeat SBP$130mmHgorDBP$80mmHg confirms a diagnosis ofhypertension. (C)

Goalsc A goal SBP,130 mmHg is appropriatefor most patients with diabetes. (C)

c Based on patient characteristics andresponse to therapy, higher or lowerSBP targets may be appropriate. (B)

c Patients with diabetes should be treatedto a DBP ,80 mmHg. (B)

Treatmentc Patients with a SBP of 130–139 mmHgor a DBP of 80–89 mmHgmay be givenlifestyle therapy alone for a maximumof 3 months and then, if targets are notachieved, be treated with addition ofpharmacological agents. (E)

c Patients with more severe hypertension(SBP $140 or DBP $90 mmHg) atdiagnosis or follow-up should receivepharmacologic therapy in addition tolifestyle therapy. (A)

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

c Pharmacologic therapy for patients withdiabetes and hypertension should bewith a regimen that includes either anACE inhibitor or an ARB. If one class isnot tolerated, the other should be sub-stituted. (C)

c Multiple drug therapy (two or moreagents at maximal doses) is generallyrequired to achieve blood pressuretargets. (B)

c Administer one or more antihyperten-sive medications at bedtime. (A)

c If ACE inhibitors, ARBs, or diuretics areused, kidney function and serum po-tassium levels should be monitored. (E)

c In pregnant patients with diabetes andchronic hypertension, blood pressuretarget goals of 110–129/65–79 mmHgare suggested in the interest of long-termmaternal health and minimizing im-paired fetal growth. ACE inhibitors andARBs are contraindicated during preg-nancy. (E)

Hypertension is a common comor-bidity of diabetes, affecting themajority ofpatients, with prevalence depending on

type of diabetes, age, obesity, and ethnic-ity. Hypertension is a major risk factor forboth CVD and microvascular complica-tions. In type 1 diabetes, hypertension isoften the result of underlying nephropathy,while in type 2 diabetes it usually coexistswith other cardiometabolic risk factors.Screening and diagnosis. Measurementof blood pressure in the office should bedone by a trained individual and follow theguidelines established for nondiabeticindividuals: measurement in the seatedposition, with feet on the floor and armsupported at heart level, after 5min of rest.Cuff size should be appropriate for theupper arm circumference. Elevated valuesshould be confirmed on a separate day.Because of the clear synergistic risks ofhypertension and diabetes, the diagnosticcutoff for a diagnosis of hypertension islower in people with diabetes (bloodpressure $130/80 mmHg) than thosewithout diabetes (blood pressure $140/90 mmHg) (219).

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 stud-ies in nondiabetic populations found thathome measurements may better correlatewith CVD risk than office measurements(220,221). However, the preponderanceof the clear evidence of benefits of treat-ment of hypertension in people with dia-betes is based on office measurements.Treatment goals. Epidemiologic analy-ses show that blood pressure .115/75mmHg is associated with increased car-diovascular event rates and mortality inindividuals with diabetes (219,222,223).Randomized clinical trials have demon-strated the benefit (reduction of CHDevents, stroke, and nephropathy) oflowering blood pressure to ,140 mmHgsystolic and ,80 mmHg diastolic in indi-viduals with diabetes (219,224–226). TheACCORD trial examined whether bloodpressure lowering to systolic blood pressure(SBP) ,120 mmHg provides greater car-diovascular protection than an SBP of130–140mmHg in patients with type 2 di-abetes at high risk for CVD (227). Theblood pressure achieved in the intensivegroup was 119/64 mmHg and in the stan-dard group was 133/70 mmHg; the differ-ence achieved was attained with an averageof 3.4 medications per participant in theintensive group and 2.1 in the standardtherapy group. The primary outcomewas a composite of nonfatal MI, nonfatal

stroke, and CVD death; the hazard ratiofor the primary end point in the intensivegroup was 0.88 (95% CI 0.73–1.06; P 50.20). Of the prespecified secondary endpoints, only stroke and nonfatal strokewere statistically significantly reduced byintensive blood pressure treatment, withhazard ratios of 0.59 (95% CI 0.39–0.89,P 5 0.01) and 0.63 (95% CI 0.41–0.96,P 5 0.03), respectively. If this finding isreal, the number needed to treat to preventone stroke over the course of 5 years withintensive blood pressuremanagement is 89.

In predefined subgroup analyses,there was a suggestion of heterogeneity(P5 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 SBP targetof,120mmHgmay be of benefit in thosewho are not targeting an A1C of,6% and/or that the benefit of intensive blood pres-sure management is diminished by moreintensive glycemia management targetingan A1C of ,6%.

Other recent randomized trial datainclude those of the ADVANCE trial inwhich treatment with an ACE inhibitorand a thiazide-type diuretic reducedthe rate of death but not the compositemacrovascular outcome. However, theADVANCE trial had no specified targetsfor the randomized comparison, and themean SBP in the intensive group (135mmHg) was not as low as the mean SBP inthe ACCORD standard-therapy group(228). A post hoc analysis of blood pressurecontrol in 6,400 patients with diabetes andCAD enrolled in the International Verapa-mil/Trandolapril Study (INVEST) demon-strated that “tight control” (,130 mmHg)was not associated with improved cardio-vascular outcomes compared with “usualcare” (130–140 mmHg) (229).

It is possible that lowering SBP fromthe low-130s to ,120 mmHg does notfurther reduce coronary events or death,and thatmost of the benefit from loweringblood pressure is achieved by targeting agoal,140 mmHg. However, this has notbeen formally assessed. Only the ACCORDblood pressure trial has formally examinedtreatment targets significantly ,130mmHg in diabetes. The absence of signifi-cant harms, the trends toward benefit in


Position Statement

stroke, and the potential heterogeneitywith respect to intensive glycemia manage-ment suggests that previously recommen-ded targets are reasonable pending furtheranalyses and results. SBP targets more orless stringent than ,130 mmHg may beappropriate for individual patients, basedon response to therapy, medication toler-ance, and individual characteristics, keepingin mind that most analyses have suggestedthat outcomes are worse if the SBP is.140mmHg.Treatment strategies. Although thereare no well-controlled studies of dietand exercise in the treatment of hyperten-sion in individuals with diabetes, the Di-etary Approaches to Stop Hypertension(DASH) study in nondiabetic individualshas shown antihypertensive effects similarto pharmacologic monotherapy. Lifestyletherapy consists of reducing sodium intake(to ,1,500 mg per day) and excess bodyweight; increasing consumption of fruits,vegetables (8–10 servings per day), andlow-fat dairy products (2–3 servings perday); avoiding excessive alcohol consump-tion (no more than two servings per day inmen and no more than one serving perday in women) (230); and increasing ac-tivity levels (219). These nonpharmaco-logical strategies may also positively affectglycemia and lipid control. Their effects oncardiovascular events have not been estab-lished. An initial trial of nonpharmacologictherapy may be reasonable in diabetic indi-viduals with mild hypertension (SBP 130–139 mmHg or DBP 80–89 mmHg). If theblood pressure is $140 mmHg systolicand/or $90 mmHg diastolic at the timeof diagnosis, pharmacologic therapyshould be initiated along with nonpharma-cologic therapy (219).

Lowering of blood pressure with reg-imens based on a variety of antihyperten-sive drugs, including ACE inhibitors,ARBs, b-blockers, diuretics, and calciumchannel blockers, has been shown to beeffective in reducing cardiovascular events.Several studies suggested that ACE inhibi-tors may be superior to dihydropyridinecalcium channel blockers in reducing car-diovascular events (231–233). However, avariety of other studies have shown no spe-cific advantage to ACE inhibitors as initialtreatment of hypertension in the generalhypertensive population, but rather anadvantage on cardiovascular outcomesof initial therapy with low-dose thiazidediuretics (219,234,235).

In people with diabetes, inhibitors ofthe renin-angiotensin system (RAS) mayhave unique advantages for initial or early

therapy of hypertension. In a nonhyper-tension trial of high-risk individuals,including a large subset with diabetes,an ACE inhibitor reduced CVD outcomes(236). In patients with congestive heartfailure (CHF), including diabetic sub-groups, ARBs have been shown to reducemajor CVD outcomes (237–240), and intype 2 patients with significant nephropa-thy, ARBswere superior to calcium channelblockers for reducing heart failure (241).Though evidence for distinct advantagesof RAS inhibitors on CVD outcomes in di-abetes remains conflicting (224,235), thehigh CVD risks associated with diabetes,and the high prevalence of undiagnosedCVD, may still favor recommendationsfor their use as first-line hypertension ther-apy in people with diabetes (219).

Recently, the blood pressure arm ofthe ADVANCE trial demonstrated thatroutine administration of a fixed combi-nation of the ACE inhibitor perindopriland the diuretic indapamide significantlyreduced combined microvascular andmacrovascular outcomes, as well as CVDand total mortality. The improved out-comes could also have been due to lowerachieved blood pressure in the perindopril-indapamide arm (228). In addition theACCOMPLISH trial showed a decreasein morbidity and mortality in those re-ceiving benazapril and amlodipine versusbenazapril and hydrochlorothiazide. Thecompelling benefits of RAS inhibitors indiabetic patients with albuminuria or renalinsufficiency provide additional rationalefor use of these agents (see section VI.B.Nephropathy Screening and Treatment).If needed to achieve blood pressure targets,amlodipine, HCTZ, or chlorthalidone canbe added. If estimated glomerular filtrationrate (GFR) is ,30 ml/min/m2, a loop di-uretic, rather than HCTZ or chlorthatli-done should be prescribed. Titration ofand/or addition of further blood pressuremedications should bemade in timely fash-ion to overcome clinical inertia in achievingblood pressure targets.

Evidence is emerging that health in-formation technology canbeused safely andeffectively as a tool to enable attainment ofblood pressure goals. Using a telemonitor-ing intervention to direct titrations of anti-hypertensive medications between medicaloffice visits has been demonstrated to have aprofound impact on SBP control (242).

An important caveat is that mostpatients with hypertension require mul-tidrug therapy to reach treatment goals,especially diabetic patientswhose targets arelower (219). If blood pressure is refractory

to optimal doses of at least 3 antihyperten-sive agents of different classifications, oneof which should be a diuretic, cliniciansshould consider an evaluation for sec-ondary forms of hypertension. Growingevidence suggests that there is an associ-ation between increase in sleep-timeblood pressure and incidence of CVDevents. A recent RCT of 448 participantswith type 2 diabetes and hypertensiondemonstrated reduced cardiovascularevents and mortality with median follow-up of 5.4 years if at least one antihyperten-sive medication was given at bedtime (243).

During pregnancy in diabetic womenwith chronic hypertension, target bloodpressure goals of SBP 110–129 mmHgand DBP 65–79 mmHg are reasonable,as they 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. Antihy-pertensive drugs known to be effective andsafe in pregnancy include methyldopa, la-betalol, diltiazem, clonidine, and prazosin.Chronic diuretic use during pregnancy hasbeen associated with restricted maternalplasma volume, whichmight reduce utero-placental perfusion (244).

2. Dyslipidemia/lipid managementRecommendations

Screeningc In most adult patients, measure fastinglipid profile at least annually. In adultswith low-risk lipid values (LDL choles-terol,100mg/dL,HDL cholesterol.50mg/dL, and triglycerides ,150 mg/dL),lipid assessments may be repeated every2 years. (E)

Treatment recommendations andgoalsc Lifestyle modification focusing on thereduction of saturated fat, trans fat, andcholesterol intake; increase of n-3 fattyacids, viscous fiber and plant stanols/sterols; weight loss (if indicated); andincreased physical activity should berecommended to improve the lipidprofile in patients with diabetes. (A)

c Statin therapy should be added to life-style therapy, regardless of baselinelipid levels, for diabetic patients:

○ with overt CVD. (A)○ without CVD who are over the age of 40years and who have one or more otherCVD risk factors. (A)

c For patients at lower risk than thoseabove (e.g., those without overt CVD


Position Statement

and under the age of 40 years), statintherapy should be considered in addi-tion to lifestyle therapy if LDL choles-terol remains .100 mg/dL or in thosewith multiple CVD risk factors. (E)

c In individuals without overt CVD, theprimary goal is an LDL cholesterol,100mg/dL (2.6 mmol/L). (A)

c In individuals with overt CVD, a lowerLDL cholesterol goal of ,70 mg/dL(1.8 mmol/L), using a high dose of astatin, is an option. (B)

c If drug-treated patients do not reachthe above targets on maximal toleratedstatin therapy, a reduction in LDLcholesterol of;30–40% from baselineis an alternative therapeutic goal. (A)

c Triglycerides levels,150 mg/dL (1.7mmol/L) and HDL cholesterol .40mg/dL (1.0 mmol/L) in men and .50mg/dL (1.3 mmol/L) in women, are de-sirable. However, LDL cholesterol–targeted statin therapy remains thepreferred strategy. (C)

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)

c Statin therapy is contraindicated in preg-nancy. (B)

Evidence for benefits of lipid-loweringtherapy. Patients with type 2 diabetes havean increased prevalence of lipid abnormal-ities, contributing to their high risk ofCVD. For the past decade or more,multiple clinical trials demonstrated sig-nificant effects of pharmacologic (primarilystatin) therapy on CVD outcomes in sub-jects with CHD and for primary CVD pre-vention (245). Subanalyses of diabeticsubgroups of larger trials (246–250) and tri-als specifically in subjects with diabetes(251,252) showed significant primary andsecondary prevention of CVD events 1/2CHDdeaths in diabetic populations. Similarto findings in nondiabetic subjects, reduc-tion in “hard” CVD outcomes (CHD deathand nonfatal MI) can be more clearly seenin diabetic subjects with high baselineCVD risk (known CVD and/or very highLDL cholesterol levels), but overall thebenefits of statin therapy in people withdiabetes at moderate or high risk for CVDare convincing.

Low levels of HDL cholesterol, oftenassociated with elevated triglyceride levels,are the most prevalent pattern of dyslipi-demia in persons with type 2 diabetes.

However, the evidence base for drugs thattarget these lipid fractions is significantlyless robust than that for statin therapy(253). Nicotinic acid has been shown toreduce CVD outcomes (254), althoughthe study was done in a nondiabetic co-hort. Gemfibrozil has been shown to de-crease rates of CVD events in subjectswithout diabetes (255,256) and in the di-abetic subgroup of one of the larger trials(255). However, in a large trial specific todiabetic patients, fenofibrate failed to re-duce overall cardiovascular outcomes(257).

Dyslipidemia treatment and targetlipid levels. For most patients with di-abetes, the first priority of dyslipidemiatherapy (unless severe hypertriglyceride-mia is the immediate issue) is to lowerLDL cholesterol to a target goal of ,100mg/dL (2.60 mmol/L) (258). Lifestyle in-tervention, including MNT, increasedphysical activity, weight loss, and smok-ing cessation, may allow some patients toreach lipid goals. Nutrition interventionshould be tailored according to each pa-tient’s age, type of diabetes, pharmacolog-ical treatment, lipid levels, and othermedical conditions and should focus onthe reduction of saturated fat, cholesterol,and trans unsaturated fat intake and increa-ses in n-3 fatty acids, viscous fiber (such asin oats, legumes, citrus), and plant stanols/sterols. Glycemic control can also benefi-ciallymodify plasma lipid levels, particularlyin patients with very high triglycerides andpoor glycemic control.

In those with clinical CVD or who areover 40 years of age with other CVD riskfactors, pharmacological treatmentshould be added to lifestyle therapyregardless of baseline lipid levels. Statinsare the drugs of choice for lowering LDLcholesterol.

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 2patients under the age of 40 years or fortype 1 patients of any age. In the HeartProtection Study (lower age limit: 40 years),the subgroup of;600 patients with type 1diabetes had a reduction in risk propor-tionately similar to that of patients withtype 2 diabetes, although not statisticallysignificant (247). Although the data are

not definitive, consideration should begiven to lipid-lowering goals in type 1 di-abetic patients similar to those in type 2diabetic patients, particularly if they haveother cardiovascular risk factors.

Alternative LDL cholesterol goals. Vir-tually all trials of statins and CVD out-comes tested specific doses of statinsagainst placebo, other doses of statin, orother statins, rather than aiming for specificLDL cholesterol goals (259). Placebo-controlled trials generally achieved LDLcholesterol reductions of 30–40% frombaseline. Hence, LDL cholesterol lower-ing of this magnitude is an acceptableoutcome for patients who cannot reachLDL cholesterol goals due to severe base-line elevations in LDL cholesterol and/orintolerance of maximal, or any, statindoses. Additionally for those with baselineLDL cholesterol minimally .100 mg/dL,prescribing statin therapy to lower LDLcholesterol ;30–40% from baseline isprobably more effective than prescrib-ing just enough to get LDL cholesterolslightly ,100 mg/dL.

Recent clinical trials in high-risk pa-tients, such as those with acute coronarysyndromes or previous cardiovascularevents (260–262), have demonstratedthat more aggressive therapy with highdoses of statins to achieve an LDL cho-lesterol of,70 mg/dL led to a significantreduction in further events. Therefore, areduction in LDL cholesterol to a goal of,70 mg/dL is an option in very-high-risk diabetic patients with overt CVD(263).

In individual patients, LDL choles-terol lowering with statins is highly vari-able and this variable response is poorlyunderstood (264). Reduction of CVDevents with statins correlates very closelywith LDL cholesterol lowering (245).When maximally tolerated doses of sta-tins fail to significantly lower LDL choles-terol (,30% reduction from patientsbaseline), the primary aim of combinationtherapy should be to achieve additionalLDL cholesterol lowering. Niacin, fenofi-brate, ezetimibe, and bile acid sequestrantsall offer additional LDL cholesterol lower-ing. The evidence that combination therapyfor LDL cholesterol lowering provides a sig-nificant increment in CVD risk reductionover statin therapy alone is still elusive.Some experts recommend a greater focuson non–HDL cholesterol and apolipopro-tein B (apoB) in patients who are likely tohave small LDL particles, such as peoplewith diabetes (265).


Position Statement

Treatment of other lipoprotein fractionsor targets. Severe hypertriglyceridemiamay warrant immediate therapy of thisabnormality with lifestyle and usuallypharmacologic therapy (fibric acid deriv-ative, niacin, or fish oil) to reduce the riskof acute pancreatitis. In the absence ofsevere hypertriglyceridemia, therapytargeting HDL cholesterol or triglycerideshas intuitive appeal but lacks the evidencebase of statin therapy. If the HDL choles-terol is,40mg/dL and the LDL cholesterol100–129 mg/dL, gemfibrozil or niacinmight be used, especially if a patient isintolerant to statins. Niacin is the mosteffective drug for raising HDL choles-terol. It can significantly increase bloodglucose at high doses, but recent studiesdemonstrate that at modest doses (750–2,000mg/day), significant improvementsin LDL cholesterol, HDL cholesterol, andtriglyceride levels are accompanied byonly modest changes in glucose that aregenerally amenable to adjustment of dia-betes therapy (266,267).Combination therapy. Combinationtherapy, with a statin and a fibrate orstatin and niacin, may be efficacious fortreatment for all three lipid fractions, butthis combination is associated with anincreased risk for abnormal transaminaselevels, myositis, or rhabdomyolysis. Therisk of rhabdomyolysis is higher withhigher doses of statins and with renalinsufficiency and seems to be lower whenstatins are combined with fenofibratethan gemfibrozil (268). In the recentACCORD study, the combination of fe-nofibrate and simvastatin did not reducethe rate of fatal cardiovascular events,nonfatal MI, or nonfatal stroke, as com-pared with simvastatin alone, in patientswith type 2 diabetes whowere at high riskfor CVD. However, prespecified sub-group analyses suggested heterogeneityin treatment effects according to sex,with a benefit of combination therapyfor men and possible harm for women,and a possible benefit for patients withboth triglyceride level $204 mg/dL andHDL cholesterol level#34 mg/dL (269).The AIM-HIGH trial randomized over3,000 patients (about one-third with di-abetes) to statin therapy plus or minusaddition of extended release niacin. Thetrial was halted early due to no differencein the primary CVD outcome and a pos-sible increase in ischemic stroke in thoseon combination therapy (270). Table 11summarizes common treatment goalsfor A1C, blood pressure, and LDL cho-lesterol.

3. Antiplatelet agentsRecommendationsc Consider aspirin therapy (75–162mg/day) as a primary prevention strategyin those with type 1 or type 2 diabetes atincreased cardiovascular risk (10-yearrisk.10%). This includesmostmen.50years of age or women.60 years of agewho have at least one additional majorrisk factor (family history of CVD, hy-pertension, smoking, dyslipidemia, oralbuminuria). (C)

c Aspirin should not be recommendedfor CVD prevention for adults withdiabetes at low CVD risk (10-yearCVD risk ,5%, such as in men ,50years and women ,60 years with nomajor additional CVD risk factors),since the potential adverse effectsfrom bleeding likely offset the potentialbenefits. (C)

c In patients in these age-groups withmultiple other risk factors (e.g., 10-yearrisk 5–10%), clinical judgment is re-quired. (E)

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

c For patients with CVD and documentedaspirin allergy, clopidogrel (75 mg/day)should be used. (B)

c Combination therapywithASA (75–162mg/day) and clopidogrel (75 mg/day) isreasonable for up to a year after an acutecoronary syndrome. (B)

Aspirin has been shown to be effectivein reducing cardiovascular morbidity andmortality in high-risk patients with pre-vious MI or stroke (secondary prevention).Its net benefit in primary preventionamong patients with no previous cardio-vascular events is more controversial, bothfor patients with and without a history ofdiabetes (271). Two recent RCTs of aspirinspecifically in patients with diabetes failedto show a significant reduction in CVD endpoints, raising further questions about theefficacy of aspirin for primary prevention inpeople with diabetes (272,273).

The Antithrombotic Trialist (ATT) col-laborators recently published an individualpatient-level meta-analysis of the six largetrials of aspirin for primary prevention inthe general population. These trials collec-tively enrolled over 95,000 participants,including almost 4,000 with diabetes.Overall, they found that aspirin reducedthe risk of vascular events by 12% (relativerisk [RR] 0.88, 95% CI 0.82–0.94). Thelargest reduction was for nonfatal MI with

little effect onCHDdeath (RR 0.95, 95%CI0.78–1.15) or total stroke. There was someevidence of a difference in aspirin effect bygender. Aspirin significantly reduced CHDevents in men but not in women. Con-versely, aspirin had no effect on stroke inmen but significantly reduced stroke inwomen. Notably, differences betweensexes in aspirin’s effects have not been ob-served in studies of secondary prevention(271). In the six trials examined by theATT collaborators, the effects of aspirinon major vascular events were similar forpatients with or without diabetes (RR0.88, 95% CI 0.67–1.15, and 0.87, 0.79–0.96), respectively. The confidence intervalwas wider for those with diabetes becauseof 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.1% per year, the numberof CVD events prevented will be similar toor greater than the number of episodes ofbleeding induced, although these compli-cations do not have equal effects on long-term health (274).

In 2010, a position statement of theADA, AHA, and the American College ofCardiology Foundation (ACCF) updatedprior joint recommendations for primaryprevention (275). Low-dose (75–162mg/day) aspirin use for primary preven-tion is reasonable for adults with diabetesand no previous history of vascular diseasewho are at increasedCVD risk (10-year riskof CVD events.10%) and who are not at

Table 11dSummary of recommendationsfor glycemic, blood pressure, and lipidcontrol for most adults with diabetes

A1C ,7.0%*Blood pressure ,130/80 mmHg†LipidsLDL 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/lifeexpectancy, comorbid conditions, known CVD oradvancedmicrovascular complications, hypoglycemiaunawareness, individual and patient considerations.†Based on patient characteristics and response totherapy, higher or lower SBP targets may be appro-priate. ‡In individuals with overt CVD, a lower LDLcholesterol goal of ,70 mg/dL (1.8 mmol/L), usinga high dose of a statin, is an option.


Position Statement

increased 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, dyslipide-mia,) family history of premature CVD, oralbuminuria.

However, aspirin is no longer recom-mended for those at low CVD risk (womenunder age 60 years and men under age 50years with no major CVD risk factors; 10-year CVD risk ,5%), as the low benefit islikely to be outweighed by the risks of sig-nificant bleeding.Clinical judgment shouldbe used for those at intermediate risk(younger patients with one or risk factors,or older patients with no risk factors; thosewith 10-year CVD risk of 5–10%) until fur-ther research is available. Use of aspirin inpatients under the age of 21 years is contra-indicated due to the associated risk ofReye’s syndrome.

Average daily dosages used in mostclinical trials involving patients with di-abetes ranged from 50 to 650mg but weremostly in the range of 100 to 325 mg/day.There is little evidence to support anyspecific dose, but using the lowest possi-ble dosage may help reduce side-effects(276). Although platelets from patientswith diabetes have altered function, it isunclear what, if any, impact that findinghas on the required dose of aspirin for car-dioprotective effects in the patient with di-abetes. There are many alternate pathwaysfor platelet activation that are independentof thromboxane A2 and thus not sensitiveto the effects of aspirin (277). Therefore,while “aspirin resistance” appears higherin the diabetic patients when measuredby a variety of ex vivo and in vitro methods(platelet aggrenometry, measurement ofthromboxane B2), these observations aloneare insufficient to empirically recommendhigher doses of aspirin be used in the di-abetic patient at this time.

Clopidogrel has been demonstratedto reduce CVD events in diabetic individ-uals (278). 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 cessationRecommendations

c Advise all patients not to smoke. (A)c Include smoking cessation counselingand other forms of treatment as a rou-tine component of diabetes care. (B)

A large body of evidence from epide-miological, case-control, and cohort studies

provides convincing documentation of thecausal link between cigarette smoking andhealth risks. Much of the work document-ing the impact of smoking on health doesnot separately discuss results on subsets ofindividuals with diabetes, but suggests thatthe identified risks are at least equivalentto those found in the general population.Other studies of individuals with diabetesconsistently demonstrate that smokershave a heightened risk of CVD and pre-mature death and increased rate of mi-crovascular complications of diabetes.Smoking may have a role in the develop-ment of type 2 diabetes.

The routine and thorough assessmentof tobacco use is important as a means ofpreventing smoking or encouraging cessa-tion. A number of large randomized clinicaltrials have demonstrated the efficacy andcost-effectiveness of brief counseling insmoking cessation, including the use ofquit lines, in the reduction of tobacco use.For the patient motivated to quit, the addi-tion of pharmacological therapy to counsel-ing is more effective than either treatmentalone. Special considerations should in-clude assessment of the level of nicotinedependence, which is associated with dif-ficulty in quitting and relapse (279).

5. CHD screening and treatmentRecommendationsScreeningc In asymptomatic patients, routinescreening for CAD is not recommended,as it does not improve outcomes as longas CVD risk factors are treated. (A)

Treatmentc In patients with known CVD, considerACE inhibitor therapy (C) and use aspirinand statin therapy (A) (if not contra-indicated) to reduce the risk of cardio-vascular events. In patients with a priorMI, b-blockers should be continued forat least 2 years after the event. (B)

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

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

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 arecently updated consensus statement(177). To identify the presence of CAD indiabetic patients without clear or suggestivesymptoms, a risk factor–based approach tothe initial diagnostic evaluation and

subsequent follow-up has intuitive appeal.However, recent studies concluded that us-ing this approach fails to identify whichpatients with type 2 diabetes will have si-lent ischemia on screening tests (182,280).

Candidates for cardiac testing includethose with 1) typical or atypical cardiacsymptoms and 2) an abnormal restingECG. The screening of asymptomatic pa-tients remains controversial. Intensive med-ical therapy, which would be indicatedanyway for diabetic patients at high risk forCVD, seems to provide equal outcomes toinvasive revascularization, which raisesquestions of how screening results wouldchange management. (281,282). There isalso some evidence that silent myocardialischemia may reverse over time, adding tothe controversy concerning aggressivescreening strategies (283). Finally, a recentrandomized observational trial demon-strated no clinical benefit to routine screen-ing of asymptomatic patients with type 2diabetes and normal ECGs (284). Despiteabnormal myocardial perfusion imaging inmore than one in five patients, cardiac out-comes were essentially equal (and very low)in screened versus unscreened patients. Ac-cordingly, theoverall effectiveness, especiallythe cost-effectiveness, of such an indiscrim-inate screening strategy is now questioned.

Newer noninvasive CAD screeningmethods, such as computed tomography(CT) and CT angiography have gained inpopularity. These tests infer the presenceof coronary atherosclerosis by measuringthe amount of calcium in coronary arteriesand, in some circumstances, by directvisualization of luminal stenoses. Althoughasymptomatic diabetic patients found tohave a higher coronary disease burden havemore future cardiac events (285–287), therole of these tests beyond risk stratificationis not clear. Their routine use leads to radi-ation exposure and may result in unneces-sary invasive testing such as coronaryangiography and revascularization proce-dures. The ultimate balance of benefit,cost, and risks of such an approach inasymptomatic patients remains controver-sial, particularly in the modern setting ofaggressive CVD risk factor control.

In all patients with diabetes, cardio-vascular risk factors should be assessed atleast annually. These risk factors includedyslipidemia, hypertension, smoking, apositive family history of premature coro-nary disease, and the presence of micro- ormacroalbuminuria. Abnormal risk factorsshould be treated as described elsewhere inthese guidelines. Patients at increased CHDrisk should receive aspirin and a statin, and


Position Statement

ACE inhibitor or ARB therapy if hyperten-sive, unless there are contraindications to aparticular drug class. While clear benefitexists for ACE inhibitor andARB therapy inpatients with nephropathy or hyperten-sion, the benefits in patients with CVD inthe absence of these conditions is less clear,especially when LDL cholesterol is con-comitantly controlled (288,289).

B. Nephropathy screening andtreatmentRecommendationsGeneral recommendationsc To reduce the risk or slow the pro-gression of nephropathy, optimize glu-cose control. (A)

c To reduce the risk or slow the pro-gression of nephropathy, optimize bloodpressure control. (A)

Screeningc Perform an annual test to assess urinealbumin excretion in type 1 diabeticpatients with diabetes duration of $5years and in all type 2 diabetic patientsstarting at diagnosis. (B)

c Measure serum creatinine at least annu-ally in all adults with diabetes regardlessof the degree of urine albumin excretion.The serum creatinine should be used toestimateGFRand stage the level of chronickidney disease (CKD), if present. (E)

Treatmentc In the treatment of the nonpregnantpatient withmicro- ormacroalbuminuria,either ACE inhibitors or ARBs should beused. (A)

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

c Reduction of protein intake to 0.8–1.0g z kg body wt21 z day21 in individualswith diabetes and the earlier stages ofCKD and to 0.8 g z kg bodywt21 z day21

in the later stages of CKD may improvemeasures of renal function (urine albu-min excretion rate, GFR) and is recom-mended. (B)

c WhenACE inhibitors, ARBs, or diureticsare used, monitor serum creatinine andpotassium levels for the development ofincreased creatinine and hyperkalemia.(E)

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

c When estimated GFR is ,60 ml z min/1.73m2, evaluate andmanage potentialcomplications of CKD. (E)

c Consider referral to a physician expe-rienced in the care of kidney diseasefor uncertainty about the etiology of

kidney disease, difficult managementissues, or advanced kidney disease. (B)

Diabetic nephropathy occurs in 20–40% of patients with diabetes and is thesingle leading cause of end-stage renaldisease (ESRD). Persistent albuminuriain the range of 30–299 mg/24 h (micro-albuminuria) has been shown to be theearliest stage of diabetic nephropathy intype 1 diabetes and a marker for develop-ment of nephropathy in type 2 diabetes.Microalbuminuria is also a well-establishedmarker of increased CVD risk (290,291).Patients with microalbuminuria whoprogress to macroalbuminuria ($300mg/24 h) are likely to progress to ESRD(292,293).However, a number of interven-tions have been demonstrated to reducethe risk and slow the progression of renaldisease.

Intensive diabetes management withthe goal of achieving near-normoglycemiahas been shown in large prospectiverandomized studies to delay the onsetof microalbuminuria and the progression ofmicro- tomacroalbuminuria in patients withtype 1 (294,295) and type 2 (73,74,78,79)diabetes. The UKPDS provided strong evi-dence that control of blood pressure can re-duce the development of nephropathy(224). In addition, large prospective ran-domized studies in patients with type 1diabetes have demonstrated that achieve-ment of lower levels of SBP (,140mmHg)resulting from treatment using ACE inhib-itors provides a selective benefit over otherantihypertensive drug classes in delayingthe progression frommicro- to macroalbu-minuria and can slow the decline in GFR inpatients with macroalbuminuria (296–298). In type 2 diabetes with hypertensionand normoalbuminuria, RAS inhibitionhas been demonstrated to delay onsetof microalbuminuria in two studies(299,300). In the latter study, there wasan unexpected higher rate of fatal cardio-vascular events with olmesartan among pa-tients with preexisting CHD.

ACE inhibitors have been shown toreducemajorCVDoutcomes (i.e.,MI, stroke,death) in patients with diabetes (236), thusfurther supporting the use of these agentsin patients with microalbuminuria, a CVDrisk factor. ARBs donot preventmicroalbu-minuria in normotensive patients with type1 or type 2 diabetes (301,302); however,ARBs have been shown to reduce the rate ofprogression from micro- to macroalbumi-nuria as well as ESRD in patients with type2 diabetes (303–305). Some evidence sug-gests that ARBs have a smaller magnitude

of rise in potassium compared with ACEinhibitors in people with nephropathy(306,307). Combinations of drugs thatblock the rennin-angiotensin-aldosteronesystem (e.g., an ACE inhibitor plus anARB, a mineralocorticoid antagonist, or adirect renin inhibitor) have been shown toprovide additional lowering of albuminuria(308–311). However, the long-term effectsof such combinations on renal or cardiovas-cular outcomes have not yet been evaluatedin clinical trials and they are associated withincreased risk for hyperkalemia.

Other drugs, such as diuretics, cal-cium channel blockers, and b-blockers,should be used as additional therapy tofurther lower blood pressure in patientsalready treated with ACE inhibitors orARBs (241), or as alternate therapy inthe rare individual unable to tolerateACE inhibitors 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 (312–315). 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 (315).

Assessment of albuminuria statusand renal function. Screening formicroalbuminuria can be performed bymeasurement of the albumin-to-creatinineratio in a random spot collection; 24-h ortimed collections are more burdensomeand add little to prediction or accuracy(316,317). Measurement of a spot urinefor albumin only, whether by immuno-assay or by using a dipstick test specificfor microalbumin, without simultaneouslymeasuring urine creatinine, is somewhatless expensive but susceptible to false-negative and false-positive determinationsas a result of variation in urine concentra-tion due to hydration and other factors.

Table 12dDefinitions of abnormalities inalbumin excretion

CategorySpot collection (mg/mg

creatinine)

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


Position Statement

Abnormalities of albumin excretionare defined in Table 12. Because of vari-ability in urinary albumin excretion(UAE), two of three specimens collectedwithin a 3- to 6-month period should beabnormal before considering a patient tohave crossed one of these diagnosticthresholds. Exercise within 24 h, infec-tion, fever, CHF, marked hyperglycemia,and marked hypertension may elevateUAE over baseline values.

Information on presence of abnormalUAE in addition to level of GFR may beused to stage CKD. The National KidneyFoundation classification (Table 13) isprimarily based on GFR levels and there-fore differs from other systems in whichstaging is based primarily on UAE (318).Studies have found decreased GFR in theabsence of increased UAE in a substantialpercentage of adults with diabetes (319).Serum creatinine should therefore be mea-sured at least annually in all adults withdiabetes, regardless of the degree of UAE.

Serum creatinine should be used toestimate GFR and to stage the level of CKD,if present. Estimated GFR (eGFR) is com-monly co-reported by laboratories, or canbe estimated using formulae such as theModification of Diet in Renal Disease(MDRD) study equation (320). Recent re-ports have indicated that the MDRD ismore accurate for the diagnosis and strati-fication of CKD in patients with diabetesthan the Cockcroft-Gault equation (321).GFR calculators are available at http://www.nkdep.nih.gov.

The role of continued annual quanti-tative assessment of albumin excretionafter diagnosis of microalbuminuria andinstitution of ACE inhibitor or ARB ther-apy and blood pressure control is unclear.Continued surveillance can assess bothresponse to therapy and progression ofdisease. Some suggest that reducing ab-normal albuminuria (.30mg/g) to the nor-mal or near-normal range may improverenal and cardiovascular prognosis, butthis approach has not been formally evalu-ated in prospective trials.

Complications of kidney disease cor-relate with level of kidney function.Whenthe eGFR is,60 mL/min/1.73 m2, screen-ing for complications of CKD is indicated(Table 14). Early vaccination against hepa-titis B is indicated in patients likely to prog-ress to end-stage kidney disease.

Consider referral to a physician expe-rienced in the care of kidney disease whenthere is uncertainty about the etiology ofkidney disease (heavy proteinuria, activeurine sediment, absence of retinopathy,rapid decline in GFR, resistant hyperten-sion).Other triggers for referralmay includedifficult management issues (anemia, sec-ondary hyperparathyroidism, metabolicbone disease, or electrolyte disturbance),or advanced kidney disease. The thresholdfor referral may vary depending on thefrequency with which a provider encoun-ters diabetic patients with significantkidney disease. Consultation with a ne-phrologist when Stage 4CKDdevelops hasbeen found to reduce cost, improve qualityof care, and keep people off dialysis longer(322). However, nonrenal specialists

should not delay educating their patientsabout the progressive nature of diabetickidney disease; the renal preservation ben-efits of aggressive treatment of blood pres-sure, blood glucose, and hyperlipidemia;and the potential need for renal replace-ment therapy.

C. Retinopathy screening andtreatmentRecommendations

General recommendationsc To reduce the risk or slow theprogressionof retinopathy, optimize glycemic con-trol. (A)

c To reduce the risk or slow the pro-gression of retinopathy, optimize bloodpressure control. (A)

Screeningc Adults and children aged 10 years orolder with type 1 diabetes should havean initial dilated and comprehensiveeye examination by an ophthalmologistor optometrist within 5 years after theonset of diabetes. (B)

c 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)

c 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 required

Table 13dStages 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. 317.

Table 14dManagement of CKD in diabetes

GFR Recommended

All patients Yearly measurement of creatinine, UAE, potassium45-60 Referral to nephrology if possibility for nondiabetic kidney disease exists

(duration type 1 diabetes ,10 years, heavy proteinuria, abnormal findingson renal ultrasound, resistant hypertension, rapid fall in GFR, or activeurinary sediment on ultrasound)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 counseling

30–44 Monitor eGFR every 3 monthsMonitor electrolytes, bicarbonate, calcium, phosphorus, parathyroidhormone, hemoglobin, albumin, weight every 3–6 monthsConsider need for dose adjustment of medications

,30 Referral to nephrologistsAdapted from National Kidney Foundation guidelines (available at http://www.kidney.org/professionals/KDOQI/guideline_diabetes/).


Position Statement

more frequently if retinopathy is pro-gressing. (B)

c High-quality fundus photographs candetect most clinically significant diabeticretinopathy. Interpretation of the imagesshould be performed by a trained eyecare provider. While retinal photogra-phy may serve as a screening tool forretinopathy, it is not a substitute for acomprehensive eye exam, which shouldbe performed at least initially and at in-tervals thereafter as recommended by aneye care professional. (E)

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

Treatmentc Promptly refer patients with any levelof macular edema, severe NPDR, or anyPDR to an ophthalmologist who isknowledgeable and experienced in themanagement and treatment of diabeticretinopathy. (A)

c Laser photocoagulation therapy is in-dicated to reduce the risk of vision lossin patients with high-risk PDR, clini-cally significant macular edema, and incases of severe NPDR. (A)

c The presence of retinopathy is not acontraindication to aspirin therapy forcardioprotection, as this therapy doesnot increase the risk of retinal hem-orrhage. (A)

Diabetic retinopathy is a highly spe-cific vascular complication of both type 1and type 2diabetes,with prevalence stronglyrelated to the duration of diabetes. Diabeticretinopathy is the most frequent cause ofnew cases of blindness among adults aged20–74 years. Glaucoma, cataracts, and otherdisorders of the eye occur earlier and morefrequently in people with diabetes.

In addition to duration of diabetes,other factors that increase the risk of, orare associated with, retinopathy includechronic hyperglycemia (323), nephropa-thy (324), and hypertension (325). Inten-sive diabetes management with the goal ofachieving near normoglycemia has beenshown in large prospective randomizedstudies to prevent and/or delay the onsetand progression of diabetic retinopathy(61,73,74,80). Lowering blood pressure

has been shown to decrease the progres-sion of retinopathy (224), although tighttargets (systolic,120 mmHg) do not im-part additional benefit (80). Several caseseries and a controlled prospective studysuggest that pregnancy in type 1 diabetic pa-tients may aggravate retinopathy (326,327);laser photocoagulation surgery can mini-mize this risk (327).

One of the main motivations forscreening for diabetic retinopathy is theestablished efficacy of laser photocoagu-lation surgery in preventing visual loss.Two large trials, the Diabetic RetinopathyStudy (DRS) in patients with PDR and theEarly Treatment Diabetic RetinopathyStudy (ETDRS) in patients with macularedema, provide the strongest support forthe therapeutic benefits of photocoagu-lation surgery. The DRS (328) showedthat panretinal photocoagulation surgeryreduced the risk of severe vision loss fromPDR from 15.9% in untreated eyes to6.4% in treated eyes, with greatest risk-to-benefit ratio in those with baseline dis-ease (disc neovascularization or vitreoushemorrhage).

The ETDRS (329) established the ben-efit of focal laser photocoagulation surgeryin eyes with macular edema, particularlythose with clinically significant macularedema, with reduction of doubling of thevisual angle (e.g., 20/50 to 20/100) from20% in untreated eyes to 8% in treatedeyes. The ETDRS also verified the benefitsof panretinal photocoagulation for high-risk PDR, and in older-onset patients withsevere NPDR or less-than-high-risk PDR.

Laser photocoagulation surgery inboth trials was beneficial in reducing therisk of further visual loss, but generallynot beneficial in reversing already dimin-ished acuity. Recombinant monoclonalantibody to vascular endothelial growthfactor is an emerging therapy that seemsto halt progression of macular edema andmay in fact improve vision in some patients(330).

The preventive effects of therapy andthe fact that patients with PDR or macularedema may be asymptomatic providestrong support for a screening program todetect diabetic retinopathy. As retinopa-thy is estimated to take at least 5 years todevelop after the onset of hyperglycemia,patients with type 1 diabetes should havean initial dilated and comprehensive eyeexamination within 5 years after the onsetof diabetes. Patients with type 2 diabetes,who generally have had years of undiag-nosed diabetes and who have a significantrisk of prevalent diabetic retinopathy at

the time of diabetes diagnosis, shouldhave an initial dilated and comprehensiveeye examination soon after diagnosis.Examinations should be performed byan ophthalmologist or optometrist who isknowledgeable and experienced in diag-nosing the presence of diabetic retinopathyand is aware of its management. Subse-quent examinations for type 1 and type 2diabetic patients are generally repeatedannually. Less-frequent exams (every 2–3years) may be cost-effective after one ormore normal eye exams, and in a popula-tion with well-controlled type 2 diabetestherewas essentially no risk of developmentof significant retinopathy with a 3-year in-terval after a normal examination (331).Examinations will be required more fre-quently if retinopathy is progressing (332).

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 (333). In-personexams are still necessary when the photosare unacceptable and for follow-up of de-tected abnormalities. Photos are not asubstitute for a comprehensive eye exam,which should be performed at least initiallyand at intervals thereafter as recommendedby an eye care professional. Results of eyeexaminations should be documented andtransmitted to the referring health care pro-fessional.

D. Neuropathy screening andtreatmentRecommendationsc All patients should be screened for distalsymmetric polyneuropathy (DPN) start-ing at diagnosis of type 2 diabetes and5 years after the diagnosis of type 1 di-abetes and at least annually thereafter,using simple clinical tests. (B)

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

c Screening for signs and symptoms ofcardiovascular autonomic neuropathyshould be instituted at diagnosis of type2 diabetes and 5 years after the diagnosisof type 1diabetes. Special testing is rarelyneeded and may not affect managementor outcomes. (E)

c Medications for the relief of specificsymptoms related to painful DPN andautonomicneuropathy are recommended,as they improve the quality of life of thepatient. (E)


Position Statement

The diabetic neuropathies are hetero-geneous with diverse clinical manifesta-tions. They may be focal or diffuse. Mostcommon among the neuropathies arechronic sensorimotor DPN and autonomicneuropathy. Although DPN is a diagnosisof exclusion, complex investigations toexclude other conditions are rarely needed.

The early recognition and appropriatemanagement of neuropathy in the patientwith diabetes is important for a number ofreasons: 1) nondiabetic neuropathies maybe present in patients with diabetes andmay be treatable; 2) a number of treatmentoptions exist for symptomatic diabetic neu-ropathy; 3) up to 50% of DPN may beasymptomatic and patients are at risk forinsensate injury to their feet; 4) autonomicneuropathy and particularly cardiovascularautonomic neuropathy is associated withsubstantial morbidity and even mortality.Specific treatment for the underlying nervedamage is currently not available, otherthan improved glycemic control, whichmay modestly slow progression (79) butnot reverse neuronal loss. Effective symp-tomatic treatments are available for somemanifestations of DPN (334) and auto-nomic neuropathy.

Diagnosis of neuropathy

Distal symmetric polyneuropathyPatients with diabetes should be screenedannually for DPN using tests such aspinprick sensation, vibration perception(using a 128-Hz tuning fork), 10-g mono-filament pressure sensation at the distalplantar aspect of both great toes and meta-tarsal joints, and assessment of ankle re-flexes. Combinations of more than one testhave .87% sensitivity in detecting DPN.Loss of 10-g monofilament perception andreduced vibration perception predict footulcers (335). Importantly, in patients withneuropathy, particularly when severe, cau-ses other than diabetes should always beconsidered, such as neurotoxicmediations,heavy metal poisoning, alcohol abuse, vita-min B12 deficiency (especially in those tak-ing metformin for prolonged periods(336), renal disease, chronic inflammatorydemyelinating neuropathy, inherited neu-ropathies, and vasculitis (337).

Diabetic autonomic neuropathy (338)The symptoms and signs of autonomicdysfunction should be elicited carefullyduring the history and physical examina-tion. Major clinical manifestations of di-abetic autonomic neuropathy includeresting tachycardia, exercise intolerance,orthostatic hypotension, constipation,

gastroparesis, erectile dysfunction, sudomo-tor dysfunction, impaired neurovascularfunction, and potentially autonomic fail-ure in response to hypoglycemia.

Cardiovascular autonomic neuropathy(CAN), a CVD risk factor (93), is the moststudied and clinically important form ofdiabetic autonomic neuropathy. CAN maybe indicated by resting tachycardia (.100bpm) or orthostasis (a fall in SBP .20mmHg upon standing without an appro-priate heart rate response); it is also associ-ated with increased cardiac event rates.Although some societies have developedguidelines for screening for CAN, thebenefits of sophisticated testing beyondrisk stratification are not clear (339).

Gastrointestinal neuropathies (e.g.,esophageal enteropathy, gastroparesis,constipation, diarrhea, fecal incontinence)are common, and any section of the gas-trointestinal tract may be affected. Gastro-paresis should be suspected in individualswith erratic glucose control or with uppergastrointestinal symptoms without otheridentified cause. Evaluation of solid-phasegastric emptying using double-isotopescintigraphy may be done if symptomsare suggestive, but test results often corre-late poorly with symptoms. Constipation isthe most common lower-gastrointestinalsymptombut can alternatewith episodes ofdiarrhea.

Diabetic autonomic neuropathy isalso associated with genitourinary tractdisturbances. In men, diabetic autonomicneuropathy may cause erectile dysfunc-tion and/or retrograde ejaculation. Eval-uation of bladder dysfunction should beperformed for individuals with diabeteswho have recurrent urinary tract infections,pyelonephritis, incontinence, or a palpablebladder.

Symptomatic treatments

DPNThe first step in management of patientswith DPN should be to aim for stable andoptimal glycemic control. Although con-trolled trial evidence is lacking, severalobservational studies suggest that neuro-pathic symptoms improve not only withoptimization of control, but also withthe avoidance of extreme blood glucosefluctuations. Patients with painful DPNmay benefit from pharmacological treat-ment of their symptoms; many agents haveconfirmed or probable efficacy confirmedin systematic reviews of RCTs (334), withseveral U.S. Food and Drug Administra-tion (FDA)-approved for the manage-ment of painful DPN.

Autonomic neuropathyGastroparesis symptoms may improvewith dietary changes and prokinetic agentssuch as metoclopramide or erythromy-cin. Treatments for erectile dysfunctionmay include phosphodiesterase type 5inhibitors, intracorporeal or intraurethralprostaglandins, vacuum devices, or penileprostheses. Interventions for other mani-festations of autonomic neuropathy aredescribed in an ADA statement on neu-ropathy (335). As with DPN treatments,these interventions do not change the un-derlying pathology and natural history ofthe disease process, but may have a pos-itive impact on the quality of life of thepatient.

E. Foot careRecommendationsc For all patients with diabetes, performan annual comprehensive foot exami-nation to identify risk factors predictiveof ulcers and amputations. The footexamination should include inspection,assessment of foot pulses, and testing forloss of protective sensation (10-g mono-filament plus testing any one of the fol-lowing: vibration using 128-Hz tuningfork, pinprick sensation, ankle reflexes,or vibration perception threshold). (B)

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

c A multidisciplinary approach is recom-mended for individuals with foot ulcersand high-risk feet, especially thosewith ahistory of prior ulcer or amputation. (B)

c 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)

c Initial screening for peripheral arterialdisease (PAD) should include a his-tory for claudication and an assess-ment of the pedal pulses. Considerobtaining an ankle-brachial index (ABI),as many patients with PAD are asymp-tomatic. (C)

c Refer patients with significant claudi-cation or a positive ABI for further vas-cular assessment and consider exercise,medications, and surgical options. (C)

Amputation and foot ulceration, con-sequences 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.


Position Statement

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

c Previous amputationc Past foot ulcer historyc Peripheral neuropathyc Foot deformityc Peripheral vascular diseasec Visual impairmentc Diabetic nephropathy (especially patientson dialysis)

c Poor glycemic controlc Cigarette smoking

Many studies have been publishedproposing a range of tests thatmightusefullyidentify patients at risk for foot ulceration,creating confusion among practitioners as towhich screening tests should be adopted inclinical practice. An ADA task force wastherefore assembled in 2008 to conciselysummarize recent literature in this area andthen recommend what should be includedin the comprehensive foot exam for adultpatients with diabetes. Their recommenda-tions are summarized below, but cliniciansshould refer to the task force report (340) forfurther details and practical descriptions ofhow to perform components of the compre-hensive foot examination.

At least annually, all adults with di-abetes should undergo a comprehensivefoot examination to identify high risk con-ditions. Clinicians should ask about historyof previous foot ulceration or amputation,neuropathic or peripheral vascular symp-toms, impaired vision, tobacco use, andfoot care practices. A general inspectionof skin integrity and musculoskeletaldeformities should be done in a well-litroom. Vascular assessment would includeinspection and assessment of pedal pulses.

The neurologic exam recommendedis designed to identify loss of protectivesensation (LOPS) rather than early neu-ropathy. The clinical examination to identifyLOPS is simple and requires no expensiveequipment. Five simple clinical tests (useof a 10-g monofilament, vibration testingusing a 128-Hz tuning fork, tests of pin-prick sensation, ankle reflex assessment,and testing vibration perception thresholdwith a biothesiometer), each with evidencefrom well-conducted prospective clinicalcohort studies, are considered useful in thediagnosis of LOPS in the diabetic foot. Thetask force agrees that any of the five testslisted could be used by clinicians to identifyLOPS, although ideally two of these shouldbe regularly performed during the screeningexamdnormally the 10-g monofilament

and one other test. One or more abnormaltests would suggest LOPS, while at least twonormal tests (and no abnormal test) wouldrule out LOPS. The last test listed, vibrationassessment using a biothesiometer or sim-ilar instrument, is widely used in the U.S.;however, identification of the patient withLOPS can easily be carried out without thisor other expensive equipment.

Initial screening for PAD should in-clude a history for claudication and anassessment of the pedal pulses. A diag-nostic ABI should be performed in anypatient with symptoms of PAD. Due tothe high estimated prevalence of PAD inpatients with diabetes and the fact thatmany patients with PAD are asymptom-atic, an ADA consensus statement on PAD(341) suggested that a screening ABI beperformed in patients over 50 years of ageand be considered in patients under 50years of agewhohave other PAD risk factors(e.g., smoking, hypertension, hyperlipid-emia, or duration of diabetes.10 years).Refer patients with significant symptomsor a positive ABI for further vascular as-sessment and consider exercise, medica-tions, and surgical options (341).

Patients with diabetes and high-riskfoot conditions should be educated re-garding their risk factors and appropriatemanagement. Patients at risk should un-derstand the implications of the loss ofprotective sensation, the importance of footmonitoring on a daily basis, the proper careof the foot, including nail and skin care,and the selection of appropriate footwear.Patients with loss of protective sensationshould be educated on ways to substituteother sensory modalities (hand palpation,visual inspection) for surveillance of earlyfoot problems. The patients’ understand-ing of these issues and their physical abil-ity to conduct proper foot surveillanceand care should be assessed. Patientswith visual difficulties, physical con-straints preventing movement, or cogni-tive problems that impair their ability toassess the condition of the foot and to in-stitute appropriate responses will needother people, such as family members,to assist in their care.

People with neuropathy or evidenceof increased plantar pressure (e.g., erythema,warmth, callus, or measured pressure) maybe adequately managed with well-fittedwalking shoes or athletic shoes that cushionthe feet and redistribute pressure. Calluscan be debridedwith a scalpel by a foot carespecialist or other health professional withexperience and training in foot care. Peoplewith bony deformities (e.g., hammertoes,

prominent metatarsal heads, bunions) mayneed extra-wide or -depth shoes. Peoplewith extreme bony deformities (e.g., Char-cot foot) who cannot be accommodatedwith commercial therapeutic footwear mayneed custom-molded shoes.

Foot ulcers and wound care may re-quire care by a podiatrist, orthopedic orvascular surgeon, or rehabilitation specialistexperienced in the management of individ-uals with diabetes.

VII. ASSESSMENTOF COMMONCOMORBID CONDITIONS

Recommendationsc For patients with risk factors, signs orsymptoms, consider assessment andtreatment for commondiabetes-associatedconditions (see Table 15). (B)

In addition to the commonly appre-ciated comorbidities of obesity, hyperten-sion, and dyslipidemia, diabetes is alsoassociated with other diseases or conditionsat rates higher than those of age-matchedpeople without diabetes. A few of the morecommon comorbidities are describedherein, and listed in Table 15.

Hearing impairmentHearing impairment, both high frequencyand low/mid frequency, is more commonin people with diabetes, perhaps due toneuropathy and/or vascular disease. In anNHANES analysis, hearing impairmentwas about twice as great in people withdiabetes than in those without diabetes,after adjusting for age and other riskfactors for hearing impairment (342).Controlling for age, race, and other demo-graphic factors, high-frequency loss inthose with diabetes was significantly asso-ciated with history of CHD and with pe-ripheral neuropathy, while low/midfrequency loss was associated with lowHDL cholesterol and with poor reportedhealth status (343).

Table 15dCommon comorbidities forwhich increased risk is associated withdiabetes

Hearing impairmentObstructive sleep apneaFatty liver diseaseLow testosterone in menPeriodontal diseaseCertain cancersFracturesCognitive impairment


Position Statement

Obstructive sleep apneaAge-adjusted rates of obstructive sleepapnea, a risk factor for CVD, are signifi-cantly higher (4- to 10-fold) with obesity,especially with central obesity, in menand women (344). The prevalence in gen-eral populations with type 2 diabetes maybe up to 23% (345) and in obese partic-ipants enrolled in the Look AHEAD trialexceeded 80% (346). Treatment of sleepapnea significantly improves quality oflife and blood pressure control. The evi-dence for a treatment effect on glycemiccontrol is mixed (347).

Fatty liver diseaseUnexplained elevation of hepatic trans-aminase concentrations are significantlyassociated with higher BMI, waist circum-ference, triglycerides, and fasting insulinand with lower HDL cholesterol. Type 2diabetes and hypertension are indepen-dently associated with transaminase ele-vations in women (348). In a prospectiveanalysis, diabetes was significantly associ-ated with incident nonalcoholic chronicliver disease and with hepatocellular car-cinoma (349). Interventions that improvemetabolic abnormalities in patients withdiabetes (weight loss, glycemic control,treatment with specific drugs for hyper-glycemia or dyslipidemia) are also benefi-cial for fatty liver disease (350).

Low testosterone in menMean levels of testosterone are lower inmenwith diabetes compared with age-matchedmenwithout diabetes, but obesity is amajorconfounder (351). The issue of treatment inasymptomatic men is controversial. Theevidence for effects of testosterone re-placement on outcomes is mixed, and re-cent guidelines suggest that screeningand treatment of men without symptomsis not recommended (352).

Periodontal diseasePeriodontal disease is more severe, butnot necessarily more prevalent, in pa-tients with diabetes than those without(353). Numerous studies have suggestedassociations with poor glycemic control,nephropathy, and CVD, but most studiesare highly confounded. A comprehensiveassessment, and treatment of identifieddisease, is indicated in patients with dia-betes, but the evidence that periodontaldisease treatment improves glycemiccontrol is mixed. A meta-analysis re-ported a significant 0.47% improvementin A1C, but noted multiple problemswith the quality of the published studies

included in the analysis (354). Severalhigh-quality RCTs have not shown a sig-nificant effect (355).

CancerDiabetes (possibly only type 2 diabetes) isassociated with increased risk of cancersof the liver, pancreas, endometrium, colon/rectum, breast, and bladder (356). The as-sociation may result from shared risk fac-tors between type 2 diabetes and cancer(obesity, age, physical inactivity) but mayalso be due to hyperinsulinemia or hyper-glycemia (356a). Patients with diabetesshould be encouraged to undergo recom-mended age- and sex-appropriate cancerscreenings and to reduce their modifiablecancer risk factors (obesity, smoking, phys-ical inactivity).

FracturesAge-matched hip fracture risk is signifi-cantly increased in both type 1 (summaryRR 6.3) and type 2 diabetes (summaryRR 1.7) in both sexes (357). Type 1 di-abetes is associated with osteoporosis, butin type 2 diabetes an increased risk of hipfracture is seen despite higher bonemineraldensity (BMD) (358). One study showedthat prevalent vertebral fractures were sig-nificantly more common in men andwomen with type 2 diabetes, but werenot associated with BMD (359). In threelarge observational studies of older adults,femoral neck BMD T-score and the WorldHealth Organization Fracture Risk Algo-rithm (FRAX) score were associatedwith hip and nonspine fracture, althoughfracture risk was higher in diabetic partic-ipants compared with participants withoutdiabetes for a given T-score and age or for agiven FRAX score risk (360). It is appropri-ate to assess fracture history and risk factorsin older patients with diabetes and to rec-ommend BMD testing if appropriate for thepatient’s age and sex. For at-risk patients,it is reasonable to consider standard pri-mary or secondary prevention strategies(reduce risk factors for falls, ensure ade-quate calcium and vitamin D intake, andavoid use of medications that lower BMD,such as glucocorticoids) and to considerpharmacotherapy for high-risk patients.For patients with type 2 diabetes withfracture risk factors, avoidance of TZDsis warranted.

Cognitive impairmentDiabetes is associated with significantly in-creased risk of cognitive decline, a greaterrate of cognitive decline, and increased riskof dementia (361,362). In a 15-year

prospective study of a community-dwell-ing people over the age of 60 years, thepresence of diabetes at baseline signifi-cantly increased the age- and sex-adjustedincidence of all-cause dementia, Alz-heimer disease, and vascular dementiacompared with rates in those with normalglucose tolerance (363). In a substudy ofthe ACCORD study, there were no differ-ences in cognitive outcomes between inten-sive and standard glycemic control,although there was significantly less of adecrement in total brain volume by MRIin participants in the intensive arm (364).The effects of hyperglycemia and insulinon the brain are areas of intense researchinterest.

VIII. DIABETES CARE INSPECIFIC POPULATIONS

A. Children and adolescents1. Type 1 diabetesThree-quarters of all cases of type 1 di-abetes are diagnosed in individuals ,18years of age. It is appropriate to considerthe unique aspects of care andmanagementof children and adolescents with type 1 di-abetes. Children with diabetes differ fromadults in many respects, including changesin insulin sensitivity related to sexual ma-turity and physical growth, ability to pro-vide self-care, supervision in child care andschool, and unique neurologic vulnerabil-ity to hypoglycemia and DKA. Attention tosuch issues as family dynamics, develop-mental stages, and physiological differen-ces related to sexual maturity are allessential in developing and implementingan optimal diabetes regimen. Although rec-ommendations for children and adoles-cents are less likely to be based on clinicaltrial evidence, expert opinion and a reviewof available and relevant experimental dataare summarized in the ADA statement oncare of children and adolescentswith type 1diabetes (365).

Ideally, the care of a child or adoles-cent with type1diabetes shouldbeprovidedby a multidisciplinary team of specialiststrained in the care of children with pediat-ric diabetes. At the very least, education ofthe child and family should be provided byhealth care providers trained and experi-enced in childhood diabetes and sensitiveto the challenges posed by diabetes in thisage-group. At the time of initial diagnosis, itis essential that diabetes education be pro-vided in a timely fashion, with the expec-tation that the balance between adultsupervision and self-care should be definedby, and will evolve according to, physical,


Position Statement

psychological, and emotional maturity.MNT and psychological support shouldbe provided at diagnosis, and regularlythereafter, by individuals experienced withthe nutritional and behavioral needs of thegrowing child and family.

a. Glycemic controlRecommendationsc Consider age when setting glycemicgoals 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 years ofage have a formof “hypoglycemic unaware-ness,” including immaturity of and a rela-tive inability to recognize and respond tohypoglycemic symptoms, placing them atgreater risk for severe hypoglycemia andits sequelae. In addition, and unlike thecase in adults, young children below theage of 5 years may be at risk for permanentcognitive impairment after episodes of severehypoglycemia (366–368). Furthermore,findings from the DCCT demonstrated thatnear-normalization of blood glucose levelswas more difficult to achieve in adolescentsthan adults. Nevertheless, the increased fre-quency of use of basal-bolus regimens andinsulin pumps in youth from infancythrough adolescence has been associatedwith more children reaching ADA blood

glucose targets (369,370) 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 documentingneurocognitive sequelae of hyperglycemiain children provide another compellingmotivation for achieving glycemic targets(371,372).

In selecting glycemic goals, the benefitson long-termhealth outcomes of achieving alower A1C should be balanced against therisks of hypoglycemia and the developmen-tal burdens of intensive regimens in childrenand youth. Age-specific glycemic and A1Cgoals are presented in Table 16.b. Screening and management ofchronic complications in children andadolescents with type 1 diabetesi. NephropathyRecommendationsc Annual screening for microalbuminuria,with a random spot urine sample for al-bumin-to-creatinine ratio (ACR), shouldbe considered once the child is 10 years ofage and has had diabetes for 5 years. (B)

c Treatment with an ACE inhibitor, ti-trated to normalization of albumin ex-cretion, should be considered whenelevated ACR is subsequently confirmedon two additional specimens from dif-ferent days. (E)

ii. HypertensionRecommendationsc Initial treatment of high-normal bloodpressure (systolic or diastolic blood pres-sure consistently above the 90th per-centile for age, sex, and height) includes

dietary intervention and exercise, aimedat weight control and increased physicalactivity, if appropriate. If target bloodpressure is not reachedwith 3–6monthsof lifestyle intervention, pharmacologictreatment should be considered. (E)

c Pharmacologic treatment of hyperten-sion (systolic or diastolic blood pressureconsistently above the 95th percentilefor age, sex, and height or consistently.130/80 mmHg, if 95% exceeds thatvalue) should be considered as soon asthe diagnosis is confirmed. (E)

c ACE inhibitors should be consideredfor the initial treatment of hypertension,following appropriate reproductivecounseling due to its potential terato-genic effects. (E)

c The goal of treatment is a blood pres-sure consistently ,130/80 mmHg orbelow the 90th percentile for age, sex,and height, whichever is lower. (E)

It is important that blood pressuremeasurements are determined correctly,using the appropriate size cuff, and withthe child seated and relaxed. Hypertensionshould be confirmed on at least 3 separatedays. Normal blood pressure levels for age,sex, and height and appropriate methodsfor determinations are available online atwww.nhlbi.nih.gov/health/prof/heart/hbp/hbp_ped.pdf.

iii. DyslipidemiaRecommendationsScreeningc If there is a family history of hypercho-lesterolemia or a cardiovascular event

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

Values by age (years)

Plasma blood glucose goal range (mg/dL)

Before meals Bedtime/overnight A1C Rationale

Toddlers andpreschoolers (0–6)

100–180 110–200 ,8.5%c Vulnerability to hypoglycemia

c Insulin sensitivity

c Unpredictability in dietary intake and physical activity

c A lower goal (,8.0%) is reasonable if it can be achievedwithout excessive hypoglycemia

School age (6–12) 90–180 100–180 ,8%c Vulnerability of hypoglycemia

c A lower goal (,7.5%) is reasonable if it can be achievedwithout excessive hypoglycemia

Adolescents and youngadults (13–19)

90–130 90–150 ,7.5%c A lower goal (,7.0%) is reasonable if it can be achievedwithout excessive hypoglycemia

Key concepts in setting glycemic goals:c Goals should be individualized and lower goals may be reasonable based on benefit-risk assessment.

c Blood glucose goals should be modified in children with frequent hypoglycemia or hypoglycemia unawareness.

c Postprandial blood glucose values should be measured when there is a discrepancy between preprandial blood glucosevalues and A1C levels and to help assess glycemia in those on basal/bolus regimens.


Position Statement

before age 55 years, or if family history isunknown, then consider obtaining afasting lipid profile on children.2 yearsof age soon after diagnosis (after glucosecontrol has been established). If familyhistory is not of concern, then considerthe first lipid screening at puberty ($10years of age). For children diagnosedwith diabetes at or after puberty, con-sider obtaining a fasting lipid profilesoon after diagnosis (after glucose con-trol has been established). (E)

c For both age-groups, if lipids are ab-normal, annual monitoring is reason-able. If LDL cholesterol values are withinthe accepted risk levels (,100 mg/dL[2.6 mmol/L]), a lipid profile repeatedevery 5 years is reasonable. (E)

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

c After the age of 10, the addition of a statinin patients who, after MNT and lifestylechanges, have LDL cholesterol .160mg/dL (4.1 mmol/L), or LDL cholesterol.130 mg/dL (3.4 mmol/L) and one ormore CVD risk factors, is reasonable. (E)

c The goal of therapy is an LDL cholesterolvalue,100 mg/dL (2.6 mmol/L). (E)

People diagnosed with type 1 diabetesin childhood have a high risk of earlysubclinical (373–375) and clinical (376)CVD. Although intervention data are lack-ing, the American Heart Association (AHA)categorizes children with type 1 diabetes inthe highest tier for cardiovascular risk andrecommends both lifestyle and pharmaco-logic treatment for those with elevated LDLcholesterol levels (377,378). Initial therapyshould be with a Step 2 AHA diet, whichrestricts saturated fat to 7% of total caloriesand restricts dietary cholesterol to 200 mgper day. Data from randomized clinical tri-als in children as young as 7months of ageindicate that this diet is safe and does notinterfere with normal growth and devel-opment (379,380).

Neither long-term safety nor cardio-vascular outcome efficacy of statin therapyhas been established for children. How-ever, recent studies have shown short-termsafety equivalent to that seen in adults, andefficacy in lowering LDL cholesterol levels,improving endothelial function, and caus-ing regression of carotid intimal thickening(381–383).No statin is approved for use un-der the age of 10 years, and statin treatmentshould generally not be used in children

with type 1 diabetes prior to this age. Forpostpubertal girls, issues of pregnancy pre-vention are paramount, since statins are cat-egoryX inpregnancy. Formore information,see section VIII.B. Preconception care.

iv. RetinopathyRecommendationsc The first ophthalmologic examinationshould be obtained once the child is$10 years of age and has had diabetesfor 3–5 years. (B)

c 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 (like albuminuria)most commonly occurs after the onset ofpuberty and after 5–10 years of diabetes du-ration (384), it has been reported in prepu-bertal children and with diabetes durationof only 1–2 years. Referrals should be madeto eye care professionals with expertise indiabetic retinopathy, an understanding ofthe risk for retinopathy in the pediatricpopulation, and experience in counselingthe pediatric patient and family on the im-portance of early prevention/intervention.

v. Celiac diseaseRecommendationsc Consider screening children with type 1diabetes for celiac disease by measuringtissue transglutaminase or anti-endomysialantibodies, with documentation of nor-mal total serum IgA levels, soon after thediagnosis of diabetes. (E)

c Testing should be considered in chil-dren with growth failure, failure to gainweight, weight loss, diarrhea, flatulence,abdominal pain, or signs of malabsorp-tion, or in children with frequent un-explained hypoglycemia or deteriorationin glycemic control. (E)

c Consider referral to a gastroenterolo-gist for evaluation with endoscopy andbiopsy for confirmation of celiac diseasein asymptomatic children with positiveantibodies. (E)

c 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. (B)

Celiac disease is an immune-mediateddisorder that occurs with increased fre-quency in patients with type 1 diabetes(1–16%of individuals comparedwith 0.3–1% in the general population) (385,386).Symptoms of celiac disease include

diarrhea, weight loss or poor weight gain,growth failure, abdominal pain, chronic fa-tigue, malnutrition due to malabsorption,and other gastrointestinal problems, andunexplained hypoglycemia or erratic bloodglucose concentrations.

Screening for celiac disease includesmeasuring serum levels of tissue transglu-taminase or anti-endomysial antibodies,then small bowel biopsy in antibody-positive children. One small study thatincluded children with and without type1 diabetes suggested that antibody-positivebut biopsy-negative children were similarclinically to those who were biopsy posi-tive, and that biopsy-negative children hadbenefits from a gluten-free diet but worsen-ing on a usual diet (387). Because this studywas small, and because children with type 1diabetes already need to follow a carefuldiet, it is difficult to advocate for not con-firming the diagnosis by biopsy beforerecommending a gluten-free diet, especiallyin asymptomatic children. In symptomaticchildren with type 1 diabetes and celiac dis-ease, gluten-free diets reduce symptomsand rates of hypoglycemia (388).

vi. HypothyroidismRecommendationsc Consider screening children with type1 diabetes for thyroid peroxidase andthyroglobulin antibodies soon afterdiagnosis. (E)

c Measuring TSH concentrations soon afterdiagnosis of type1diabetes, aftermetaboliccontrol has been established, is reasonable.If normal, consider rechecking every 1–2years, especially if the patient developssymptoms of thyroid dysfunction, thyro-megaly, or an abnormal growth rate. (E)

Autoimmune thyroid disease is themost common autoimmune disorder as-sociated with diabetes, occurring in 17–30% of patients with type 1 diabetes(389). About one-quarter of type 1 chil-dren have thyroid autoantibodies at thetime of diagnosis of their diabetes (390),and the presence of thyroid autoantibodies ispredictive of thyroid dysfunction, generallyhypothyroidism but less commonly hyper-thyroidism (391). Subclinical hypothyroid-ism may be associated with increased risk ofsymptomatic hypoglycemia (392) and withreduced linear growth (393). Hyperthyroid-ismalters glucosemetabolism, potentially re-sulting in deterioration 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 implement


Position Statement

it. Family involvement in diabetes remainsan important component of optimal di-abetes management throughout childhoodand into adolescence.Health care providerswho care for children and adolescents,therefore, must be capable of evaluatingthe behavioral, emotional, and psychosocialfactors that interfere with implementationand then must work with the individualand family to resolve problems that occurand/or to modify goals as appropriate.

d. School and day careSince 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 posi-tion statement on diabetes care in theschool and day care setting (394) for fur-ther discussion.

e. Transition from pediatric to adultcareRecommendationsc As teens transition into emerging adult-hood, health care providers and familiesmust recognize their many vulnerabilities(B) and prepare the developing teen, be-ginning in early tomid adolescence and atleast 1 year prior to the transition. (E)

c Both pediatricians and adult health careproviders should assist in providingsupport and links to resources for theteen and emerging adult. (B)

Care and close supervision of diabetesmanagement is increasingly shifted fromparents and other older adults through-out childhood and adolescence; however,the shift from pediatric to adult health careproviders often occurs very abruptly as theolder teen enters the next developmentalstage, referred to as emerging adulthood(395, 397), a critical period for young peo-ple who have diabetes. During this periodof major life transitions, youth begin tomove out of their parents’ home and mustbecome more fully responsible for their di-abetes care including the many aspects ofself management,makingmedical appoint-ments, and financing health care once theyare no longer covered under their parentshealth insurance (396,397). In addition tolapses in health care, this is also a period ofdeterioration in glycemic control, increasedoccurrence of acute complications, psy-chosocial and emotional behavioral issues,and emergence of chronic complications(396–399).

Though scientific evidence continuesto be limited, it is clear that early and

ongoing attention be given to comprehen-sive and coordinated planning for seamlesstransition of all youth from pediatric toadult health care (336,337). A comprehen-sive discussion regarding the challengesfaced during this period, including specificrecommendations is found in the ADA po-sition statement “Diabetes Care for Emerg-ing Adults: Recommendations for theTransition from Pediatric to Adult DiabetesCare Systems” (397).

TheNational Diabetes Education Pro-gram (NDEP) has materials available tofacilitate the 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 (28). Distinctionbetween type 1 and type 2 diabetes in chil-dren can be difficult, since the prevalenceof overweight in children continues to riseand since autoantigens and ketosis may bepresent in a substantial number of patientswith features of type 2 diabetes (includingobesity and acanthosis nigricans). Such adistinction at the time of diagnosis is criticalsince treatment regimens, educational ap-proaches, and dietary counsel will differmarkedly between the two diagnoses.

Type 2 diabetes has a significant in-cidence of comorbidities already pres-ent at the time of diagnosis (400). It isrecommended that blood pressure mea-surement, a fasting lipid profile,microalbu-minuria assessment, and dilated eyeexamination be performed at the time ofdiagnosis. Thereafter, screening guide-lines and treatment recommendationsfor hypertension, dyslipidemia, microal-buminuria and retinopathy in youth withtype 2 diabetes are similar to those foryouth with type 1. Additional problemsthat may need to be addressed includepolycystic ovarian disease and the vari-ous comorbidities associated with pedi-atric obesity such as sleep apnea, hepaticsteatosis, orthopedic complications, andpsychosocial concerns. An ADA consensusstatement on this subject (30) providesguidance on the prevention, screening,and treatment of type 2 diabetes and itscomorbidities in young people.

3. Monogenic diabetes syndromesMonogenic forms of diabetes (neonataldiabetes or maturity-onset diabetes ofyouth) represent a small fraction of chil-dren with diabetes (,5%), but the readyavailability of commercial genetic testing isnow enabling a true genetic diagnosis withincreasing frequency. It is important to

correctly diagnose one of the monogenicforms of diabetes, as these children maybe incorrectly diagnosed with type 1 ortype 2 diabetes, leading to nonoptimaltreatment regimens and delays in diagnos-ing other family members.

The diagnosis of monogenic diabetesshould be considered in the followingsettings: diabetes diagnosed within thefirst 6months of life; in childrenwith strongfamily history of diabetes butwithout typicalfeatures of type 2 diabetes (nonobese, low-risk ethnic group); in children with mildfasting hyperglycemia (100–150 mg/dL[5.5–8.5 mmol]), especially if young andnonobese; and in children with diabetesbut with negative autoantibodies withoutsigns of obesity or insulin resistance. A re-cent international consensus document dis-cusses further in detail the diagnosis andmanagement of children with monogenicforms of diabetes (401).

B. Preconception careRecommendationsc A1C levels should be as close to normalas possible (,7%) in an individual pa-tient before conception is attempted. (B)

c Starting at puberty, preconception coun-seling should be incorporated in the rou-tine diabetes clinic visit for all women ofchildbearing potential. (C)

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

c Medications usedby suchwomen shouldbe evaluated prior to conception, sincedrugs commonly used to treat diabetesand its complications may be contra-indicated or not recommended in preg-nancy, including statins, ACE inhibitors,ARBs, andmost noninsulin therapies. (E)

c Since many pregnancies are unplanned,consider the potential risks and benefitsof medications that are contraindicatedin pregnancy in all women of child-bearing potential, and counsel womenusing such medications accordingly. (E)

Major congenital malformations re-main the leading cause of mortality andserious morbidity in infants of motherswith type 1 and type 2 diabetes. Observa-tional studies indicate that the risk of mal-formations increases continuously withincreasing maternal glycemia during thefirst 6–8 weeks of gestation, as definedbyfirst-trimester A1C concentrations. Thereis no threshold for A1C values belowwhich risk disappears entirely. However,


Position Statement

malformation 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 appearsto reduce the risk of congenital malforma-tions. Five nonrandomized studies com-pared rates of major malformations ininfants between women who participatedin preconception diabetes care programsand women who initiated intensive di-abetes management after they were alreadypregnant. The preconception care programswere multidisciplinary and designed totrain patients in diabetes self-managementwith diet, intensified insulin therapy, andSMBG. Goals were set to achieve normalblood glucose concentrations, and .80%of subjects achieved normal A1C concen-trations before they became pregnant. Inall five studies, the incidence of majorcongenital malformations in women whoparticipated in preconception care (range1.0–1.7% of infants) was much lowerthan the incidence in women who did notparticipate (range 1.4–10.9% of infants)(94). One limitation of these studies isthat participation in preconception carewas self-selected rather than randomized.Thus, it is impossible to be certain thatthe lower malformation rates resultedfully from improved diabetes care. None-theless, the evidence supports the conceptthat malformations can be reduced or pre-vented by careful management of diabetesbefore pregnancy.

Planned pregnancies greatly facilitatepreconception diabetes care. Unfortu-nately, nearly two-thirds of pregnanciesin women with diabetes are unplanned,leading to a persistent excess of malfor-mations in infants of diabetic mothers. Tominimize the occurrence of these devas-tating malformations, standard care for allwomen with diabetes who have child-bearing potential, beginning at the onsetof puberty or at diagnosis, should include1) education about the risk of malforma-tions associated with unplanned pregnan-cies and poormetabolic control; and 2) useof effective contraception at all times, un-less the patient has good metabolic controland is actively trying to conceive.

Women contemplating pregnancyneed to be seen frequently by a multidis-ciplinary team experienced in the man-agement of diabetes before and duringpregnancy. The goals of preconceptioncare are to 1) involve and empower the pa-tient in the management of her diabetes,

2) achieve the lowest A1C test results pos-sible without excessive hypoglycemia,3) assure effective contraception until stableand acceptable glycemia is achieved, and 4)identify, evaluate, and treat long-term dia-betes complications such as retinopathy,nephropathy, neuropathy, hypertension,and CHD (94).

Among the drugs commonly used inthe treatment of patients with diabetes, anumber may be relatively or absolutelycontraindicated during pregnancy. Sta-tins are category X (contraindicated foruse in pregnancy) and should be discon-tinued before conception, as should ACEinhibitors (402). ARBs are category C(risk cannot be ruled out) in the first tri-mester, but category D (positive evidenceof risk) in later pregnancy, and shouldgenerally be discontinued before preg-nancy. Since many pregnancies are un-planned, health care professionals caringfor any woman of childbearing potentialshould consider the potential risks andbenefits of medications that are contrain-dicated in pregnancy.Women usingmed-ications 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. Poten-tial risks and benefits of oral antidiabeticagents in the preconception period mustbe carefully weighed, recognizing thatdata are insufficient to establish the safetyof these agents in pregnancy.

For further discussion of preconcep-tion care, see the ADA consensus statementon preexisting diabetes and pregnancy (94)and also the position statement (403) onthis subject.

C. Older adultsRecommendationsc Older adults who are functional, cog-nitively intact, and have significant lifeexpectancy should receive diabetes careusing goals developed for youngeradults. (E)

c Glycemic goals for older adults notmeeting the above criteria may be re-laxed using individual criteria, but hy-perglycemia leading to symptoms or riskof acute hyperglycemic complicationsshould be avoided in all patients. (E)

c Other cardiovascular risk factors shouldbe treated in older adults with con-sideration of the time frame of benefitand the individual patient. Treatmentof hypertension is indicated in virtuallyall older adults, and lipid and aspirin

therapy may benefit those with life ex-pectancy at least equal to the time frameof primary or secondary preventiontrials. (E)

c Screening for diabetes complicationsshould be individualized in older adults,but particular attention should be paidto complications that would lead tofunctional impairment. (E)

Diabetes is an important health con-dition for the aging population; at least20% of patients over the age of 65 yearshave diabetes, and this number can beexpected to grow rapidly in the comingdecades. Older individuals with diabeteshave higher 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 commongeriatric syndromes, such as polyphar-macy, depression, cognitive impairment,urinary incontinence, injurious falls, andpersistent pain.

The American Geriatric Society’sguidelines for improving the care of theolder person with diabetes (404) haveinfluenced the following discussion andrecommendations. The care of older adultswith diabetes is complicated by their clini-cal and functional heterogeneity. Someolder individuals developed diabetes yearsearlier and may have significant complica-tions; others who are newly diagnosedmayhave had years of undiagnosed diabeteswith resultant complications or may havefew complications from the disease. Someolder adults with diabetes are frail and haveother underlying chronic conditions, sub-stantial diabetes-related comorbidity, orlimited physical or cognitive functioning.Other older individuals with diabeteshave little comorbidity and are active. Lifeexpectancies are highly variable for thispopulation, but often longer than cliniciansrealize. Providers caring for older adultswith diabetes must take this heterogeneityinto consideration when setting and prior-itizing 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.


Position Statement

For patients with advanced diabetescomplications, life-limiting comorbid ill-ness, or substantial cognitive or functionalimpairment, it is reasonable to set less in-tensive glycemic target goals. These patientsare less likely to benefit from reducing therisk of microvascular complications andmore likely to suffer serious adverse effectsfrom hypoglycemia. However, patientswith poorly controlled diabetes may besubject to acute complications of diabe-tes, including dehydration, poor woundhealing, and hyperglycemic hyperosmo-lar coma. Glycemic goals at a minimumshould avoid these consequences.

Although control of hyperglycemiamay be important in older individualswith diabetes, greater reductions in mor-bidity and mortality may result from con-trol of other cardiovascular risk factorsrather than from tight glycemic controlalone. There is strong evidence fromclinical trials of the value of treating hyper-tension in the elderly (405,406). There isless evidence for lipid-lowering and aspirintherapy, although the benefits of these in-terventions for primary and secondary pre-vention are likely to apply to older adultswhose life expectancies equal or exceed thetime frames seen in clinical trials.

Special care is required in prescribingandmonitoring pharmacologic therapy inolder adults. Metformin is often contra-indicated because of renal insufficiency orsignificant heart failure. TZDs can causefluid retention, which may exacerbate orlead to heart failure. They are contraindi-cated in patients with CHF (New YorkHeart Association Class III and IV), and ifused at all should be used very cautiouslyin those with, or at risk for, milder degreesof CHF. Sulfonylureas, other insulin secre-tagogues, and insulin can cause hypogly-cemia. Insulin use requires that patients orcaregivers have good visual and motorskills and cognitive ability. Drugs shouldbe started at the lowest dose and titrated upgradually until targets are reached or sideeffects develop.

Screening for diabetes complicationsin older adults also should be individual-ized. Particular attention should be paidto complications that can develop over shortperiods of time and/or that would signifi-cantly impair functional status, such as visualand lower extremity complications.

D. Cystic fibrosis–related diabetes(CFRD)Recommendationsc Annual screening for CFRD with OGTTshould begin by age 10 years in all

patients with cystic fibrosis who do nothaveCFRD (B). Use of A1C as a screeningtest for CFRD is not recommended. (B)

c During a period of stable health thediagnosis of CFRD can bemade in cysticfibrosis patients according to usual di-agnostic criteria. (E)

c Patients with CFRD should be treatedwith insulin to attain individualizedglycemic goals. (A)

c Annual monitoring for complicationsof diabetes is recommended, beginning5 years after the diagnosis of CFRD. (E)

CFRD is the most common comorbid-ity in personswith cystic fibrosis, occurringin about 20% of adolescents and 40–50%of adults. The additional diagnosis of dia-betes in this population is associated withworse nutritional status, more severe in-flammatory lung disease, and greater mor-tality from respiratory failure. Insulininsufficiency related to partial fibrotic de-struction of the islet mass is the primarydefect in CFRD. Genetically determinedfunction of the remaining b-cells and insu-lin resistance associated with infection andinflammation may also play a role. Encour-aging new data suggest that early detectionand aggressive insulin therapy have nar-rowed the gap in mortality between cysticfibrosis patients with and without diabetes,and have eliminated the difference in mor-tality between the sexes (407).

Recommendations for the clinicalmanagement of CFRD can be found in arecent ADA position statement on thistopic (408).

IX. DIABETES CARE INSPECIFIC SETTINGS

A. Diabetes care in the hospitalRecommendationsc All patients with diabetes admitted tothe hospital should have their diabetesclearly identified in the medical record.(E)

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

c Goals for blood glucose levels:

○ Critically ill patients: Insulin therapyshould be initiated for treatment of persis-tent hyperglycemia starting at a threshold ofno greater than 180 mg/dL (10 mmol/L).Once insulin therapy is started, a glu-cose range of 140–180 mg/dL (7.8 to 10

mmol/L) is recommended for the ma-jority of critically ill patients. (A)

○ More stringent goals, such as 110–140mg/dL (6.1–7.8 mmol/L) may be appro-priate for selected patients, as long as thiscan be achieved without significant hy-poglycemia. (C)

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

○ Non–critically ill patients: There is noclear evidence for specific blood glucosegoals. If treated with insulin, premealblood glucose targets generally ,140mg/dL (7.8 mmol/L) with randomblood glucose ,180 mg/dL (10.0mmol/L) are reasonable, provided thesetargets can be safely achieved. Morestringent targets may be appropriate instable patients with previous tight glyce-mic control. Less stringent targets may beappropriate in those with severe co-morbidities. (E)

c Scheduled subcutaneous insulin withbasal, nutritional, and correction com-ponents is the preferred method forachieving and maintaining glucose con-trol in noncritically ill patients.

c Glucose monitoring should be initiatedin any patient not known to be diabeticwho receives therapy associated withhigh-risk for hyperglycemia, includinghigh-dose glucocorticoid therapy, ini-tiation of enteral or parenteral nutrition,or other medications such as octreotideor immunosuppressive medications. (B)If hyperglycemia is documented andpersistent, consider treating such pa-tients to the same glycemic goals as pa-tients with known diabetes. (E)

c A hypoglycemia management protocolshould be adopted and implementedby each hospital or hospital system. Aplan for preventing and treating hypo-glycemia should be established for eachpatient. Episodes of hypoglycemia inthe hospital should be documented inthe medial record and tracked. (E)

c Consider obtaining an A1C on patientswith diabetes admitted to the hospital ifthe result of testing in the previous 2–3months is not available. (E)

c Patients with hyperglycemia in the hos-pital who do not have a prior diagnosisof diabetes should have appropriateplans for follow-up testing and caredocumented at discharge. (E)


Position Statement

Hyperglycemia in the hospital canrepresent previously known diabetes,previously undiagnosed diabetes, orhospital-related hyperglycemia (fastingblood glucose $126 mg/dL or randomblood glucose $200 mg/dL occurringduring the hospitalization that revertsto normal after hospital discharge). Hyper-glycemia in the hospital is extensively re-viewed in an ADA technical review (409).An updated consensus statement by theAmerican Association of Clinical Endocri-nologists (AACE) and ADA (410) forms thebasis for the discussion and guidelines inthis section.

The management of hyperglycemia inthe hospital has often been consideredsecondary in importance to the conditionthat prompted admission (409). However, abody of literature now supports targetedglucose control in the hospital setting forpotential improved clinical outcomes. Hy-perglycemia in the hospital may result fromstress, decompensation of type 1 or type 2or other forms of diabetes, and/or may beiatrogenic due towithholding of antihyper-glycemic medications or administration ofhyperglycemia-provoking agents such asglucocorticoids or vasopressors.

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 RCTs suggested that intensivetreatment of hyperglycemia improved hos-pital outcomes (409,411,412). In general,these studies were heterogeneous in termsof patient population, blood glucose targetsand insulin protocols used, provision ofnutritional support, and the proportion ofpatients 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 (413,414) or have evenshown increased mortality risk (415).Moreover, these recent RCTs have high-lighted the risk of severe hypoglycemia re-sulting from such efforts (413–418).

The largest study to date, NICE-SUGAR, a multicenter, multinational RCT,compared the effect of intensive glycemiccontrol (target 81–108 mg/dL, mean bloodglucose attained 115 mg/dL) to standardglycemic control (target 144–180 mg/dL,mean blood glucose attained 144 mg/dL)on outcomes among 6,104 critically ill par-ticipants, almost all of whom required me-chanical ventilation (415). Ninety-daymortality was significantly higher in the in-tensive versus the conventional group in

both surgical and medical patients, as wasmortality from cardiovascular causes. Se-vere hypoglycemia was also more commonin the intensively treated group (6.8% vs.0.5%; P , 0.001). The precise reason forthe increased mortality in the tightly con-trolled group is unknown. The results ofthis study lie in stark contrast to a famous2001 single-center study which reported a42% relative reduction in ICU mortality incritically ill surgical patients treated to a tar-get blood glucose of 80–110 mg/dL (411).Importantly, the control group in NICE-SUGAR had reasonably good blood glu-cose management, maintained at a meanglucose of 144 mg/dL, only 29 mg/dLabove the intensively managed patients.Accordingly, this study’s findings do notdisprove the notion that glycemic controlin the ICU is important. However they dostrongly suggest that it may not be neces-sary to target blood glucose values ,140mg/dL, and that a highly stringent targetof,110mg/dLmay actually be dangerous.

In a recent meta-analysis of 26 trials(N5 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) (418). 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 medical and mixedcritical care settings did not. It was con-cluded that, overall, intensive insulintherapy increased the risk of hypoglyce-mia but provided no overall benefit onmortality in the critically ill, although apossible mortality benefit to patients ad-mitted to the surgical ICU was suggested.1. Glycemic targets in hospitalizedpatientsDefinition of glucose abnormalities inthe hospital setting. Hyperglycemia inthe hospital has been defined as anyblood glucose .140 mg/dL (7.8 mmol/L). Levels that are significantly and per-sistently above this may require treat-ment in hospitalized patients. A1Cvalues .6.5% suggest, in undiagnosedpatients, that diabetes preceded hospital-ization (419). Hypoglycemia has been de-fined as any blood glucose ,70 mg/dL(3.9 mmol/L). This is the standard defini-tion in outpatients and correlates with theinitial threshold for the release of counter-regulatory hormones. Severe hypoglycemia

in hospitalized patients has beendefinedbymany as ,40 mg/dL (2.2 mmol/L), al-though this is lower than the ;50 mg/dL(2.8 mmol/L) level at which cognitive im-pairment begins in normal individuals(420). As with hyperglycemia, hypoglyce-mia among inpatients is also associatedwith adverse short- and long-term out-comes. Early recognition and treatment ofmild-to-moderate hypoglycemia (40–69mg/dL (2.2–3.8 mmol/L) can prevent dete-rioration to a more severe episode with po-tential adverse sequelae (410).Critically ill patients. Based on theweight of the available evidence, for themajority of critically ill patients in the ICUsetting, insulin infusion should be usedto control hyperglycemia, with a startingthreshold of no higher than 180 mg/dL(10.0 mmol/L). Once intravenous insu-lin is started, the glucose level should bemaintained between 140 and 180 mg/dL(7.8–10.0 mmol/L). Greater benefitmaybe realized at the lower end of thisrange. Although strong evidence is lack-ing, somewhat lower glucose targetsmay be appropriate in selected patients.However, targets ,110 mg/dL (6.1mmol/L) are not recommended. Use ofinsulin infusion protocols with demon-strated safety and efficacy, resulting inlow rates of hypoglycemia, are highlyrecommended (410).Noncritically ill patients. With no pro-spective RCT data to inform specificglycemic targets in noncritically ill patients,recommendations are based on clinicalexperience and judgment. For the majorityof noncritically ill patients treated withinsulin, premeal glucose targets shouldgenerally be ,140 mg/dL (7.8 mmol/L)with random blood glucose,180 mg/dL(10.0 mmol/L), as long as these targetscan be safely achieved. To avoid hypogly-cemia, consideration should be given toreassessing the insulin regimen if bloodglucose levels fall,100 mg/dL (5.6 mmol/L). Modification of the regimen is requiredwhen blood glucose values are,70mg/dL(3.9 mmol/L), unless the event is easily ex-plained by other factors (such as a missedmeal). There is some evidence that system-atic attention to hyperglycemia in the emer-gency room leads to better glycemic controlin the hospital for those subsequently admit-ted (421).

Occasional patients with a prior his-tory of successful tight glycemic controlin the outpatient setting who are clini-cally stable may be maintained with aglucose range below the above cut points.Conversely, higher glucose ranges may be


Position Statement

acceptable in terminally ill patients or inpatients with severe comorbidities, as wellas in those in patient-care settings wherefrequent glucose monitoring or close nurs-ing 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 concurrent useof medications that might affect glucoselevels (e.g., steroids, octreotide), must beincorporated into the day-to-day decisionsregarding insulin dosing (410).2. Antihyperglycemic agents in hospi-talized patientsIn the hospital setting, insulin therapy isthe preferred method of glycemic controlin majority of clinical situations (410). 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 (422,423). Outsideof critical care units, scheduled subcuta-neous insulin that 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 in a randomized trialto be associated with adverse outcomes ingeneral surgery patients with type 2 dia-betes (424). SSI is potentially dangerousin type 1 diabetes (410). The reader is re-ferred to several recent publications andreviews that describe currently availableinsulin preparations and protocols andprovide guidance in use of insulin therapyin specific clinical settings including par-enteral nutrition (425) and enteral tubefeedings and with high-dose glucocorti-coid therapy (410).

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. Continu-ation of these agents may be appropriatein selected stable patients who are expec-ted to consume meals at regular intervals,and they may be initiated or resumed inanticipation of discharge once the patientis clinically stable. Specific caution is re-quired with metformin due to the possi-bility that a contraindication may developduring the hospitalization, such as renal

insufficiency, unstable hemodynamic sta-tus, or need for an imaging study thatrequires a radio-contrast dye.3. Preventing hypoglycemiaIn the hospital, multiple risk factors forhypoglycemia are present. Patients with orwithout diabetes may experience hypogly-cemia in the hospital in association withaltered nutritional state, heart failure, renalor liver disease, malignancy, infection, orsepsis. Additional triggering events leadingto iatrogenic hypoglycemia include suddenreduction of corticosteroid dose, alteredability of the patient to report symptoms,reduction of oral intake, emesis, new n.p.o.status, inappropriate timing of short- orrapid-acting insulin in relation to meals,reduction of rate of administration of in-travenous dextrose, and unexpected inter-ruption of enteral feedings or parenteralnutrition.

Despite the preventable nature ofmany inpatient episodes of hypoglyce-mia, institutions are more likely to havenursing protocols for the treatment ofhypoglycemia than for its prevention.Tracking such episodes and analyzingtheir causes are important quality im-provement activities (410).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 (410). In the care of di-abetes, implementation of standardizedorder sets for scheduled and correction-dose insulin may reduce reliance onsliding-scale management. As hospitalsmove to comply with “meaningful use”regulations for electronic health records,as mandated by the Health InformationTechnology Act, efforts should be madeto assure that all components of structuredinsulin order sets are incorporated intoelectronic insulin order sets (426,427).

A team approach is needed to estab-lish hospital pathways. To achieve glyce-mic targets associated with improvedhospital outcomes, hospitals will needmultidisciplinary support to develop in-sulin management protocols that effec-tively and safely enable achievement ofglycemic targets (428).5. Self-management in the hospitalSelf-management of diabetes in the hos-pital may be appropriate for competentadult patients who have a stable level of

consciousness, have reasonably stabledaily insulin requirements, successfullyconduct self-management of diabetes athome, have physical skills needed tosuccessfully self-administer insulin andperform SMBG, have adequate oral in-take, are proficient in carbohydratecounting, use multiple daily insulin in-jections or insulin pump therapy, and em-ploy sick-day management. The patientand physician, in consultation with nurs-ing staff, 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 (410). Ahospital policy and procedures delineat-ing inpatient guidelines for CSII therapyare advisable, and availability of hospitalpersonnel with expertise in CSII therapyis essential. It is important that nursingpersonnel document basal rates and bolusdoses taken on a regular basis (at leastdaily).6. MNT in the hospitalThe goals of MNT are to optimize glyce-mic control, provide adequate calories tomeet metabolic demands, and create adischarge plan for follow-up care(409,429). 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 hospitals be-cause they facilitatematching the prandialinsulin dose to the amount of carbohy-drate consumed (430). Because of thecomplexity of nutrition issues in thehospital, a registered dietitian, knowl-edgeable and skilled in MNT, shouldserve as an inpatient team member. Thedietitian is responsible for integrating in-formation about the patient’s clinical con-dition, eating, and lifestyle habits and forestablishing treatment goals in order todetermine a realistic plan for nutritiontherapy (431,432).

7. Bedside blood glucose monitoringPoint-of-care (POC) blood glucose mon-itoring 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


Position Statement

receiving nutrition, glucose monitoring isperformed every 4 to 6 h (433,434). More-frequent 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, needles, and meters toreduce the risk of transmission of bloodborne diseases. Shared lancing devices carryessentially the same risk as is conferred fromsharing of syringes and needles (435).

Accuracy of blood glucose measure-ments using POC meters has limitationsthat must be considered. Although theFDA allows a 1/2 20% error for bloodglucose meters, questions about the ap-propriateness of these criteria have beenraised (388). Glucose measures differ sig-nificantly between plasma and wholeblood, terms that are often used inter-changeably and can lead to misinterpreta-tion.Most commercially available capillaryblood glucose meters introduce a correc-tion factor of ;1.12 to report a “plasmaadjusted” value (436).

Significant discrepancies betweencapillary, venous, and arterial plasma sam-ples have been observed in patients withlow or high hemoglobin concentrations,hypoperfusion, and the presence of in-terfering substances, particularly maltose,as contained in immunoglobulins (437).Analytical variability has been describedwith several POC meters (438). Increas-ingly newer generation POC blood glu-cose meters correct for variation inhematocrit and for interfering substances.Any glucose result that does not correlatewith the patient’s status should be con-firmed through conventional laboratorysampling of plasma glucose. The FDAhas become increasingly concerned aboutthe use of POC blood glucose meters inthe hospital and is presently reviewingmatters related to their use.8. Discharge planning and DSMETransition 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 (439). It is important to re-member that diabetes discharge planningis not a separate entity, but is 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, so diabe-tes discharge planning will be limited tocommunication of medication and dietorders. For the patient who is dischargedto assisted living or to home, the optimalprogram will need to consider the typeand severity of diabetes, the effects of thepatient’s illness on blood glucose levels,and the capacities and desires of the pa-tient. Smooth transition to outpatientcare should be ensured. The Agency forHealthcare Research and Quality recom-mends that at a minimum, dischargeplans include:

c Medication reconciliation: The patient’smedications must be cross-checked toensure that no chronic medicationswere stopped and to ensure the safety ofnew prescriptions.

c Whenever possible, prescriptions fornew or changed medication should befilled and reviewedwith the patient andfamily at or before discharge.

c Structured discharge communication:Information on medication changes,pending tests and studies, and follow-up needs must be accurately andpromptly communicated to outpatientphysicians.

c Discharge summaries should be trans-mitted to the primary physician as soonas possible after discharge.

c Appointment-keeping behavior is en-hanced when the inpatient team sched-ules outpatient medical follow up priorto discharge. Ideally the inpatient careproviders or case managers/dischargeplanners will schedule follow-up visit(s) with the appropriate professionals,including the primary care provider,endocrinologist, and diabetes educator(99).

Teaching diabetes self-managementto patients in hospitals is a challengingtask. Patients are ill, under increasedstress related to their hospitalization anddiagnosis, and in an environment notconducive to learning. Ideally, peoplewith diabetes should be taught at a timeand place conducive to learningdas anoutpatient in a recognized program of di-abetes education. For the hospitalized pa-tient, diabetes “survival skills” educationis generally a feasible approach to providesufficient information and training to

enable safe care at home. Patients hospi-talized because of a crisis related to diabe-tes management or poor care at homeneed education to prevent subsequent ep-isodes of hospitalization. An assessmentof the need for a home health referral orreferral to an outpatient diabetes educa-tion program should be part of dischargeplanning for all patients.

DSME cannot wait until discharge,especially in those new to insulin therapyor in whom the diabetes regimen has beensubstantially altered during the hospital-ization.

It is recommended that the followingareas of knowledge be reviewed andaddressed prior to hospital discharge:

c Identification of health care providerwho will provide diabetes care afterdischarge

c Level of understanding related to thediagnosis of diabetes, SMBG, and ex-planation of home blood glucose goals

c Definition, recognition, treatment, andprevention of hyperglycemia and hy-poglycemia

c Information on consistent eating pat-terns

c When and how to take blood glucose–loweringmedications including insulinadministration (if going home on in-sulin)

c Sick-day managementc Proper use and disposal of needles andsyringes

It is important that patients be pro-vided with appropriate durable medicalequipment, medication, supplies, and pre-scriptions at the time of discharge in orderto avoid a potentially dangerous hiatus incare. These supplies/prescriptions shouldinclude:

c Insulin (vials or pens) if neededc Syringes or pen needles (if needed)c Oral medications (if needed)c Blood glucose meter and stripsc Lancets and lancing devicec Urine ketone strips (type 1)c Glucagon emergency kit (insulin-treated)c Medical alert application/charm

More expanded diabetes educationcan be arranged in the community. Anoutpatient follow-up visit with the pri-mary care provider, endocrinologist, ordiabetes educator within 1 month ofdischarge is advised for all patients havinghyperglycemia in the hospital. Clear com-munication with outpatient providers


Position Statement

either directly or via hospital dischargesummaries facilitates safe transitions tooutpatient care. Providing informationregarding the cause or the plan for de-termining the cause of hyperglycemia,related complications and comorbidities,and recommended treatments can assistoutpatient providers as they assume on-going care.

B. Diabetes and employmentAny person with diabetes, whether insulin-treated or noninsulin treated, should beeligible for any employment for whichhe/she is otherwise qualified. Employ-ment decisions should never be based ongeneralizations or stereotypes regardingthe effects of diabetes. When questionsarise about the medical fitness of a personwith diabetes for a particular job, a healthcare professional with expertise in treat-ing diabetes should perform an individ-ualized assessment. See the ADA positionstatement on diabetes and employment(440).

C. Diabetes and drivingA large percentage of people with diabetesin the U.S. and elsewhere seek a licenseto drive, either for personal or employ-ment purposes. There has been consider-able debate whether, and the extent towhich, diabetes may be a relevant factor indetermining the driver ability and eligi-bility for a license.

People with diabetes are subject to agreat variety of licensing requirementsapplied by both state and federal juris-dictions, which may lead to loss of em-ployment or significant restrictions on aperson’s license. Presence of a medicalcondition that can lead to significantlyimpaired consciousness or cognitionmay lead to drivers being evaluated forfitness to drive. For diabetes, this typi-cally arises when the person has had ahypoglycemic episode behind the wheel,even if this did not lead to a motor vehicleaccident.

Epidemiologic and simulator datasuggest that people with insulin-treateddiabetes have a small increase in risk ofmotor vehicle accidents, primarily due tohypoglycemia and decreased awarenessof hypoglycemia. This increase (RR 1.12–1.19) is much smaller than the risks asso-ciated with teenage male drivers (RR 42),driving at night (RR 142), driving on ruralroads comparedwith urban roads (RR 9.2),and obstructive sleep apnea (RR 2.4), allof which are accepted for unrestricted li-censure.

The ADA position statement on di-abetes and driving (441) recommendsagainst blanket restrictions based on thediagnosis of diabetes and urges individualassessment by a health care professionalknowledgeable in diabetes if restrictionson licensure are being considered. Pa-tients should be evaluated for decreasedawareness of hypoglycemia, hypoglyce-mia episodes while driving, or severe hy-poglycemia. Patients with retinopathy orperipheral neuropathy require assessmentto determine if those complications inter-fere with operation of a motor vehicle.Health care professionals should be cogni-zant of the potential risk of driving withdiabetes and counsel their patients aboutdetecting and avoiding hypoglycemiawhile driving.

D. Diabetes management incorrectional institutionsPeople with diabetes in correctional facil-ities should receive care that meets na-tional standards. Because it is estimatedthat nearly 80,000 inmates have diabetes,correctional institutions should havewritten policies and procedures for themanagement of diabetes and for trainingof medical and correctional staff in di-abetes care practices. See the ADA posi-tion statement on diabetes managementin correctional institutions (442) for fur-ther discussion.

X. STRATEGIES FORIMPROVING DIABETES CARE

Recommendationsc Care should be aligned with compo-nents of the Chronic Care Model to en-sure productive interactions between aprepared proactive practice team and aninformed activated patient. (A)

c When feasible, care systems shouldsupport team-based care, communityinvolvement, patient registries, and em-bedded decision support tools to meetpatient needs (B).

c Treatment decisions should be timelyand based on evidence-based guidelinesthat are tailored to individual patientpreferences, prognoses, and comorbid-ities. (B)

c Apatient-centered communication styleshould be employed that incorporatespatient preferences, assesses literacy andnumeracy, and addresses cultural bar-riers to care. (B)

There has been steady improvementin the proportion of diabetes patients

achieving recommended levels of A1C,blood pressure, and LDL cholesterol inthe 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 NHANES data (443). This hasbeen accompanied by improvements inlipids and blood pressure control andhas led to substantial reductions in end-stage microvascular complications inthose with diabetes. Nevertheless insome studies only 57.1% of adults withdiagnosed diabetes achieved an A1C,7%, only 45.5% had a blood pressure,130/80 mmHg, and only 46.5% had atotal cholesterol ,200 mg/dL, with only12.2% of people with diabetes achievingall three treatment goals (444). Evidencealso suggests that progress in risk factorcontrol may be slowing (445). Certain pa-tient groups, such as those with complexcomorbidities, financial or other socialhardships, and/or limited English profi-ciency (LEP), may present particular chal-lenges to goal-based care (446,447).Persistent variation in quality of diabetescare across providers and across practicesettings even after adjusting for patientfactors indicates that there remains poten-tial for substantial further improvementsin diabetes care.

While numerous interventions to im-prove adherence to the recommendedstandards have been implemented, a ma-jor barrier to optimal care is a deliverysystem that too often is fragmented, lacksclinical information capabilities, oftenduplicates services, and is poorly de-signed for the coordinated delivery ofchronic care. The Chronic Care Model(CCM) has been shown in numerousstudies to be an effective framework forimproving the quality of diabetes care(448). The CCM includes six core ele-ments for the provision of optimal careof patients with chronic disease: 1) deliv-ery system design (moving from a reactiveto a proactive care delivery system whereplanned visits are coordinated through ateam based approach), 2) self-managementsupport, 3) decision support (basingcare on evidence-based, effective careguidelines), 4) clinical information sys-tems (using registries that can providepatient-specific and population-basedsupport to the care team), 5) communityresources and policies (identifying or de-veloping resources to support healthylifestyles), and 6) health systems (tocreate a quality-oriented culture). Redef-inition of the roles of the clinic staff and


Position Statement

promoting self-management on the partof the patient are fundamental to the suc-cessful implementation of the CCM(449). Collaborative, multidisciplinaryteams are best suited to provide suchcare for people with chronic conditionslike diabetes and to facilitate patients’ per-formance of appropriate self-management(148,150,450,451).

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. Threespecific objectives, with references to lit-erature that outline practical strategies toachieve each, are below.

Objective 1: Optimize provider andteam behaviorThe care team should prioritize timelyand appropriate intensification of lifestyleand/or pharmaceutical therapy of patientswho have not achieved beneficial levels ofblood pressure, lipid, or glucose control(452). Strategies such as explicit goal set-ting with patients (453); identifying andaddressing language, numeracy, or cul-tural barriers to care (454–456); integrat-ing evidence-based guidelines and clinicalinformation tools into the process of care(457–459); and incorporating care man-agement teams including nurses, pharma-cists, and other providers (460–463) haveeach been shown to optimize providerand team behavior and thereby catalyzereduction in A1C, blood pressure, andLDL cholesterol.

Objective 2: Support patient behaviorchangeSuccessful diabetes care requires a sys-tematic approach to supporting patients’behavior change efforts, including (a)healthy lifestyle changes (physical activ-ity, healthy eating, nonuse of tobacco,weight management, effective coping),(b) disease self-management (medicationtaking and management, self-monitoringof glucose and blood pressure when clin-ically appropriate); and (c) prevention ofdiabetes complications (self-monitoringof foot health, active participation inscreening for eye, foot, and renal compli-cations, and immunizations). High-qualityDSME has been shown to improve patientself-management, satisfaction, and glucosecontrol (166,464), as has delivery of on-going diabetes self-management support(DSMS) so that gains achieved duringDSME are sustained (120,121,137). Na-tional DSME standards call for an integrated

approach that includes clinical contentand skills and behavioral strategies (goal-setting, problem solving) and addressesemotional concerns in each needed curric-ulum content area.

Objective 3: Change the systemof careThe most successful practices have aninstitutional priority for providing highquality of care (465). Changes that havebeen shown to increase quality of diabetescare include basing care on evidence-based guidelines (466), expanding therole of teams and staff (449,467), rede-signing the processes of care (468,469),implementing electronic health recordtools (470,471), activating and educatingpatients (472,473), and identifying and/or developing and engaging communityresources and public policy that supporthealthy lifestyles (474). Recent initiativessuch as the Patient Centered MedicalHome showpromise to improve outcomesthrough coordinated primary care and of-fer new opportunities for team-basedchronic disease care (475). Alterations inreimbursement that reward the provisionof appropriate and high quality care ratherthan visit-based billing (476), and that canaccommodate the need to personalize caregoals,may provide additional incentives toimprove diabetes care (477).

It is clear that optimal diabetes man-agement requires an organized, systematicapproach and involvement of a coordi-nated team of dedicated health care pro-fessionals working in an environmentwhere patient-centered high quality careis a priority.

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292. Gall MA, Hougaard P, Borch-Johnsen K,Parving HH. Risk factors for develop-ment of incipient and overt diabetic ne-phropathy in patients with non-insulindependent diabetes mellitus: prospec-tive, observational study. BMJ 1997;314:783–788

293. Ravid M, Lang R, Rachmani R, LishnerM. Long-term renoprotective effect ofangiotensin-converting enzyme inhibi-tion in non-insulin-dependent diabetesmellitus. A 7-year follow-up study. ArchIntern Med 1996;156:286–289

294. Reichard P, Nilsson BY, Rosenqvist U.The effect of long-term intensified in-sulin treatment on the development ofmicrovascular complications of diabetesmellitus. N Engl J Med 1993;329:304–309

295. The Diabetes Control and Complications(DCCT) Research Group. Effect of in-tensive therapy on the development andprogression of diabetic nephropathy inthe Diabetes Control and ComplicationsTrial. Kidney Int 1995;47:1703–1720

296. Lewis EJ, Hunsicker LG, Bain RP, RohdeRD; The Collaborative Study Group. Theeffect of angiotensin-converting-enzymeinhibition on diabetic nephropathy. NEngl J Med 1993;329:1456–1462

297. Laffel LM, McGill JB, Gans DJ; NorthAmericanMicroalbuminuria Study Group.The beneficial effect of angiotensin-converting enzyme inhibitionwith captoprilon diabetic nephropathy in normotensiveIDDM patients with microalbuminuria.Am J Med 1995;99:497–504

298. Bakris GL,WilliamsM, Dworkin L, et al.;National Kidney Foundation Hyperten-sion and Diabetes Executive CommitteesWorking Group. Preserving renal func-tion in adults with hypertension anddiabetes: a consensus approach. Am JKidney Dis 2000;36:646–661

299. Remuzzi G, Macia M, Ruggenenti P.Prevention and treatment of diabetic renaldisease in type 2 diabetes: the BENEDICT

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300. HallerH, Ito S, Izzo JL Jr, et al.; ROADMAPTrial Investigators. Olmesartan for thedelay or prevention of microalbuminuriain type 2 diabetes. N Engl J Med 2011;364:907–917

301. Bilous R, Chaturvedi N, Sjølie AK, et al.Effect of candesartan onmicroalbuminuriaand albumin excretion rate in diabetes:three randomized trials. Ann Intern Med2009;151:11–20, W3-4

302. Mauer M, Zinman B, Gardiner R, et al.Renal and retinal effects of enalapril andlosartan in type 1 diabetes. N Engl J Med2009;361:40–51

303. Lewis EJ, Hunsicker LG, Clarke WR,et al.; Collaborative Study Group. Re-noprotective effect of the angiotensin-receptor antagonist irbesartan in patientswith nephropathy due to type 2 diabetes.N Engl J Med 2001;345:851–860

304. Brenner BM, Cooper ME, de Zeeuw D,et al.; RENAAL Study Investigators. Ef-fects of losartan on renal and cardiovas-cular outcomes in patients with type 2diabetes and nephropathy. N Engl J Med2001;345:861–869

305. Parving HH, Lehnert H, Bröchner-Mortensen J, Gomis R, Andersen S,Arner P; Irbesartan in Patients with Type2 Diabetes and Microalbuminuria StudyGroup. The effect of irbesartan on thedevelopment of diabetic nephropathy inpatients with type 2 diabetes. N Engl JMed 2001;345:870–878

306. Pepine CJ, Handberg EM, Cooper-DeHoff RM, et al.; INVEST Investigators.A calcium antagonist vs a non-calciumantagonist hypertension treatment strat-egy for patients with coronary arterydisease. The International Verapamil-Trandolapril Study (INVEST): a ran-domized controlled trial. JAMA 2003;290:2805–2816

307. Bakris GL, Siomos M, Richardson D,et al.; VAL-K Study Group. ACE in-hibition or angiotensin receptor block-ade: impact on potassium in renalfailure. Kidney Int 2000;58:2084–2092

308. Mogensen CE, Neldam S, Tikkanen I,et al. Randomised controlled trial of dualblockade of renin-angiotensin systemin patients with hypertension, micro-albuminuria, and non-insulin dependentdiabetes: the candesartan and lisinoprilmicroalbuminuria (CALM) study. BMJ2000;321:1440–1444

309. Schjoedt KJ, Jacobsen P, Rossing K,Boomsma F, Parving HH. Dual blockadeof the renin-angiotensin-aldosterone sys-tem in diabetic nephropathy: the role ofaldosterone. Horm Metab Res 2005;37(Suppl 1):4–8

310. Schjoedt KJ, Rossing K, Juhl TR, et al.Beneficial impact of spironolactone indiabetic nephropathy. Kidney Int 2005;68:2829–2836

311. Parving HH, Persson F, Lewis JB, LewisEJ, Hollenberg NK; AVOID Study In-vestigators. Aliskiren combined withlosartan in type 2 diabetes and ne-phropathy. N Engl J Med 2008;358:2433–2446

312. Pijls LT, de Vries H, Donker AJ, van EijkJT. The effect of protein restrictionon albuminuria in patients with type 2diabetes mellitus: a randomized trial.Nephrol Dial Transplant 1999;14:1445–1453

313. Pedrini MT, Levey AS, Lau J, ChalmersTC, Wang PH. The effect of dietaryprotein restriction on the progression ofdiabetic and nondiabetic renal diseases:a meta-analysis. Ann Intern Med 1996;124:627–632

314. Hansen HP, Tauber-Lassen E, Jensen BR,Parving HH. Effect of dietary proteinrestriction on prognosis in patients withdiabetic nephropathy. Kidney Int 2002;62:220–228

315. Kasiske BL, Lakatua JD, Ma JZ, Louis TA.A meta-analysis of the effects of dietaryprotein restriction on the rate of declinein renal function. Am J Kidney Dis 1998;31:954–961

316. Eknoyan G, Hostetter T, Bakris GL, et al.Proteinuria and other markers of chronickidney disease: a position statement ofthe national kidney foundation (NKF)and the national institute of diabetes anddigestive and kidney diseases (NIDDK).Am J Kidney Dis 2003;42:617–622

317. Levey AS, Coresh J, Balk E, et al.; NationalKidney Foundation. National KidneyFoundation practice guidelines forchronic kidney disease: evaluation,classification, and stratification. Ann In-tern Med 2003;139:137–147

318. Kramer H, Molitch ME. Screening forkidney disease in adults with diabetes.Diabetes Care 2005;28:1813–1816

319. Kramer HJ, Nguyen QD, Curhan G, HsuCY. Renal insufficiency in the absence ofalbuminuria and retinopathy among adultswith type 2 diabetes mellitus. JAMA 2003;289:3273–3277

320. Levey AS, Bosch JP, Lewis JB, Greene T,Rogers N, Roth D; Modification of Dietin Renal Disease Study Group. A moreaccurate method to estimate glomerularfiltration rate from serum creatinine:a new prediction equation. Ann InternMed 1999;130:461–470

321. Rigalleau V, Lasseur C, Perlemoine C,et al. Estimation of glomerular filtrationrate in diabetic subjects: Cockcroft for-mula or modification of Diet in RenalDisease study equation? Diabetes Care2005;28:838–843

322. Levinsky NG. Specialist evaluation inchronic kidney disease: too little, toolate. Ann InternMed 2002;137:542–543

323. Klein R. Hyperglycemia and microvas-cular and macrovascular disease in di-abetes. Diabetes Care 1995;18:258–268


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324. Estacio RO, McFarling E, Biggerstaff S,Jeffers BW, Johnson D, Schrier RW.Overt albuminuria predicts diabetic ret-inopathy in Hispanics with NIDDM. AmJ Kidney Dis 1998;31:947–953

325. Leske MC, Wu SY, Hennis A, et al.; Bar-bados Eye Study Group. Hyperglycemia,blood pressure, and the 9-year incidenceof diabetic retinopathy: the Barbados EyeStudies. Ophthalmology 2005;112:799–805

326. Fong DS, Aiello LP, Ferris FL 3rd, KleinR. Diabetic retinopathy. Diabetes Care2004;27:2540–2553

327. Diabetes Control and ComplicationsTrial Research Group. Effect of preg-nancy on microvascular complicationsin the diabetes control and complica-tions trial. Diabetes Care 2000;23:1084–1091

328. The Diabetic Retinopathy Study Re-search Group. Preliminary report on ef-fects of photocoagulation therapy. AmJ Ophthalmol 1976;81:383–396

329. ETDRS. Photocoagulation for diabeticmacular edema. Early Treatment DiabeticRetinopathy Study report number 1. EarlyTreatment Diabetic Retinopathy Studyresearch group. Arch Ophthalmol 1985;103:1796–1806

330. Boyer DS. Ranibizumab (anti-VEGF) forvision loss due to diabetic macularedema: reslts of two phase III random-ized trials. 2011.

331. Agardh E, Tababat-Khani P. Adopting3-year screening intervals for sight-threatening retinal vascular lesions intype 2 diabetic subjects without reti-nopathy. Diabetes Care 2011;34:1318–1319

332. Fong DS, Aiello L, Gardner TW, et al.;American Diabetes Association. Reti-nopathy in diabetes. Diabetes Care 2004;27(Suppl 1):S84–S87

333. Ahmed J, Ward TP, Bursell SE, AielloLM, Cavallerano JD, Vigersky RA. Thesensitivity and specificity of nonmydriaticdigital stereoscopic retinal imaging indetecting diabetic retinopathy. DiabetesCare 2006;29:2205–2209

334. Bril V, England J, Franklin GM, et al.;American Academy of Neurology;American Association of Neuromuscularand Electrodiagnostic Medicine; Ameri-can Academy of Physical Medicine andRehabilitation. Evidence-based guide-line: Treatment of painful diabetic neu-ropathy: report of the American Academyof Neurology, the American Associationof Neuromuscular and ElectrodiagnosticMedicine, and the American Academy ofPhysical Medicine and Rehabilitation.Neurology 2011;76:1758–1765

335. Boulton AJ, Vinik AI, Arezzo JC, et al.;American Diabetes Association. Diabeticneuropathies: a statement by the Amer-ican Diabetes Association. Diabetes Care2005;28:956–962

336. Wile DJ, Toth C. Association of metfor-min, elevated homocysteine, and meth-ylmalonic acid levels and clinicallyworsened diabetic peripheral neuropa-thy. Diabetes Care 2010;33:156–161

337. Freeman R. Not all neuropathy in di-abetes is of diabetic etiology: differentialdiagnosis of diabetic neuropathy. CurrDiab Rep 2009;9:423–431

338. Vinik AI, Maser RE, Mitchell BD,Freeman R. Diabetic autonomic neu-ropathy. Diabetes Care 2003;26:1553–1579

339. Spallone V, Bellavere F, Scionti L, et al.;Diabetic Neuropathy Study Group of theItalian Society of Diabetology. Recom-mendations for the use of cardiovasculartests in diagnosing diabetic autonomicneuropathy. Nutr Metab Cardiovasc Dis2011;21:69–78

340. Boulton AJ, Armstrong DG, Albert SF,et al.; American Diabetes Association;American Association of Clinical Endo-crinologists. Comprehensive foot exam-ination and risk assessment: a report ofthe task force of the foot care interestgroup of the American Diabetes Associa-tion, with endorsement by the AmericanAssociation of Clinical Endocrinologists.Diabetes Care 2008;31:1679–1685

341. AmericanDiabetesAssociation. Peripheralarterial disease in people with diabetes.Diabetes Care 2003;26:3333–3341

342. Bainbridge KE, Hoffman HJ, Cowie CC.Diabetes and hearing impairment in theUnited States: audiometric evidencefrom the National Health and NutritionExamination Survey, 1999 to 2004. AnnIntern Med 2008;149:1–10

343. Bainbridge KE, Hoffman HJ, Cowie CC.Risk factors for hearing impairmentamong U.S. adults with diabetes: Na-tional Health and Nutrition ExaminationSurvey 1999-2004. Diabetes Care 2011;34:1540–1545

344. Li C, Ford ES, Zhao G, Croft JB, Balluz LS,Mokdad AH. Prevalence of self-reportedclinically diagnosed sleep apnea accordingto obesity status in men and women:National Health and Nutrition Examina-tion Survey, 2005-2006. Prev Med 2010;51:18–23

345. West SD, Nicoll DJ, Stradling JR. Preva-lence of obstructive sleep apnoea in menwith type 2 diabetes. Thorax 2006;61:945–950

346. Foster GD, Sanders MH, Millman R,et al.; Sleep AHEAD Research Group.Obstructive sleep apnea among obesepatients with type 2 diabetes. DiabetesCare 2009;32:1017–1019

347. Shaw JE, Punjabi NM, Wilding JP,Alberti KG, Zimmet PZ; InternationalDiabetes Federation Taskforce on Epide-miology and Prevention. Sleep-disorderedbreathing and type 2 diabetes: a reportfrom the International Diabetes Feder-ation Taskforce on Epidemiology and

Prevention. Diabetes Res Clin Pract 2008;81:2–12

348. Clark JM, Brancati FL, Diehl AM. Theprevalence and etiology of elevated ami-notransferase levels in the United States.Am J Gastroenterol 2003;98:960–967

349. El-Serag HB, Tran T, Everhart JE. Di-abetes increases the risk of chronic liverdisease and hepatocellular carcinoma.Gastroenterology 2004;126:460–468

350. American Gastroenterological Associa-tion. American Gastroenterological As-sociation medical position statement:nonalcoholic fatty liver disease. Gastro-enterology 2002;123:1702–1704

351. Dhindsa S, Miller MG, McWhirter CL,et al. Testosterone concentrations in di-abetic and nondiabetic obese men. Di-abetes Care 2010;33:1186–1192

352. Bhasin S, Cunningham GR, Hayes FJ,et al.; Task Force, Endocrine Society.Testosterone therapy in men with an-drogen deficiency syndromes: an Endo-crine Society clinical practice guideline. JClin Endocrinol Metab 2010;95:2536–2559

353. Khader YS, Dauod AS, El-Qaderi SS,Alkafajei A, Batayha WQ. Periodontalstatus of diabetics compared with non-diabetics: a meta-analysis. J DiabetesComplications 2006;20:59–68

354. Darré L, Vergnes JN, Gourdy P, SixouM.Efficacy of periodontal treatment onglycaemic control in diabetic patients:A meta-analysis of interventional stud-ies. Diabetes Metab 2008;34:497–506

355. International Diabetes Federation. OralHealth for People with Diabetes. Brussels,International Diabetes Federation, 2009

356. Suh S, Kim KW. Diabetes and cancer: isdiabetes causally related to cancer? Di-abetes Metab J 2011;35:193–198

356a. International Diabetes Federation. OralHealth for Patients with Diabetes.Brussels, 2009, International DiabetesFederation

357. Janghorbani M, Van Dam RM, WillettWC, Hu FB. Systematic review of type1 and type 2 diabetes mellitus and riskof fracture. Am J Epidemiol 2007;166:495–505

358. Vestergaard P. Discrepancies in bonemineral density and fracture risk in pa-tients with type 1 and type 2 diabetesdameta-analysis. Osteoporos Int 2007;18:427–444

359. Yamamoto M, Yamaguchi T, YamauchiM, Kaji H, Sugimoto T. Diabetic patientshave an increased risk of vertebral frac-tures independent of BMD or diabeticcomplications. J Bone Miner Res 2009;24:702–709

360. Schwartz AV, Vittinghoff E, Bauer DC,et al.; Study of Osteoporotic Fractures(SOF) Research Group; OsteoporoticFractures in Men (MrOS) ResearchGroup; Health, Aging, and Body Com-position (Health ABC) Research Group.


Position Statement

Association of BMD and FRAX scorewith risk of fracture in older adults withtype 2 diabetes. JAMA 2011;305:2184–2192

361. Cukierman T, Gerstein HC, WilliamsonJD. Cognitive decline and dementia indiabetesdsystematic overview of pro-spective observational studies. Dia-betologia 2005;48:2460–2469

362. Biessels GJ, Staekenborg S, Brunner E,Brayne C, Scheltens P. Risk of dementiain diabetes mellitus: a systematic review.Lancet Neurol 2006;5:64–74

363. Ohara T, Doi Y, Ninomiya T, et al. Glu-cose tolerance status and risk of de-mentia in the community: the Hisayamastudy. Neurology 2011;77:1126–1134

364. Launer LJ, Miller ME, Williamson JD,Lazar RM, Gerstein HC, Murray AM,Sullivan M, Horowitz KR, Ding J,Marcovina S, Lovato LC, Lovato J,Margolis KL, O’Connor P, Lipkin EW,Hirsch J, Coker L, Maldjian J, SunshineJL, Truwit C, Davatzikos C, Bryan RN:Effects of intensive glucose lowering onbrain structure and function in peoplewith type 2 diabetes (ACCORD MIND):a randomised open-label substudy.Lancet Neurol 2011;10:969–977

365. Silverstein J, Klingensmith G, CopelandKC, et al.; American Diabetes Associa-tion. Care of children and adolescentswith type 1 diabetes: a statement of theAmerican Diabetes Association. DiabetesCare 2005;28:186–212

366. Northam EA, Anderson PJ, Werther GA,Warne GL, Adler RG, Andrewes D.Neuropsychological complications ofIDDM in children 2 years after diseaseonset. Diabetes Care 1998;21:379–384

367. Rovet J, Alvarez M. Attentional func-tioning in children and adolescents withIDDM. Diabetes Care 1997;20:803–810

368. Bjørgaas M, Gimse R, Vik T, Sand T.Cognitive function in type 1 diabeticchildren with and without episodes ofsevere hypoglycaemia. Acta Paediatr1997;86:148–153

369. Nimri R, Weintrob N, Benzaquen H,Ofan R, Fayman G, Phillip M. Insulinpump therapy in youth with type 1 di-abetes: a retrospective paired study. Pe-diatrics 2006;117:2126–2131

370. Doyle EA, Weinzimer SA, Steffen AT,Ahern JA, Vincent M, Tamborlane WV.A randomized, prospective trial com-paring the efficacy of continuous sub-cutaneous insulin infusion with multipledaily injections using insulin glargine.Diabetes Care 2004;27:1554–1558

371. Perantie DC, Wu J, Koller JM, et al. Re-gional brain volume differences associatedwith hyperglycemia and severe hypogly-cemia in youth with type 1 diabetes. Di-abetes Care 2007;30:2331–2337

372. Mäkimattila S, Malmberg-Cèder K,Häkkinen AM, et al. Brain metabolic al-terations in patients with type 1 diabetes-

hyperglycemia-induced injury. J CerebBlood Flow Metab 2004;24:1393–1399

373. Krantz JS, Mack WJ, Hodis HN, Liu CR,Liu CH, Kaufman FR. Early onset ofsubclinical atherosclerosis in youngpersons with type 1 diabetes. J Pediatr2004;145:452–457

374. Järvisalo MJ, Putto-Laurila A, Jartti L,et al. Carotid artery intima-media thick-ness in children with type 1 diabetes.Diabetes 2002;51:493–498

375. Haller MJ, Samyn M, Nichols WW, et al.Radial artery tonometry demonstratesarterial stiffness in children with type 1diabetes. Diabetes Care 2004;27:2911–2917

376. Orchard TJ, Forrest KY, Kuller LH,Becker DJ; Pittsburgh Epidemiology ofDiabetes Complications Study. Lipidand blood pressure treatment goals fortype 1 diabetes: 10-year incidence datafrom the Pittsburgh Epidemiology ofDiabetes Complications Study. DiabetesCare 2001;24:1053–1059

377. Kavey RE, Allada V, Daniels SR, et al.;American Heart Association ExpertPanel on Population and PreventionScience; American Heart AssociationCouncil on Cardiovascular Disease in theYoung; American Heart AssociationCouncil on Epidemiology and Pre-vention; American Heart AssociationCouncil on Nutrition, Physical Activityand Metabolism; American Heart Asso-ciation Council on High Blood PressureResearch; American Heart AssociationCouncil on Cardiovascular Nursing;American Heart Association Councilon the Kidney in Heart Disease; Inter-disciplinary Working Group on Qualityof Care and Outcomes Research. Car-diovascular risk reduction in high-riskpediatric patients: a scientific statementfrom the American Heart AssociationExpert Panel on Population andPreventionScience; the Councils on CardiovascularDisease in the Young, Epidemiology andPrevention, Nutrition, Physical Activityand Metabolism, High Blood PressureResearch, Cardiovascular Nursing, andthe Kidney in Heart Disease; and theInterdisciplinary Working Group onQuality of Care and Outcomes Research:endorsed by the American Academy ofPediatrics. Circulation 2006;114:2710–2738

378. McCrindle BW, Urbina EM, DennisonBA, et al.; American Heart AssociationAtherosclerosis, Hypertension, andObesity in Youth Committee; AmericanHeart Association Council of Cardio-vascular Disease in the Young; AmericanHeart Association Council on Cardio-vascular Nursing. Drug therapy of high-risk lipid abnormalities in childrenand adolescents: a scientific statementfrom the American Heart Associa-tion Atherosclerosis, Hypertension, and

Obesity in Youth Committee, Council ofCardiovascular Disease in the Young,with the Council on CardiovascularNursing. Circulation 2007;115:1948–1967

379. Salo P, Viikari J, Hämäläinen M, et al.Serumcholesterol ester fatty acids in 7- and13-month-old children in a prospectiverandomized trial of a low-saturated fat,low-cholesterol diet: the STRIP babyproject. Special Turku coronary Riskfactor Intervention Project for children.Acta Paediatr 1999;88:505–512

380. The Dietary Intervention Study in Chil-dren (DISC). The Writing Group for theDISC Collaborative Research Group.Efficacy and safety of lowering dietaryintake of fat and cholesterol in childrenwith elevated low-density lipoproteincholesterol. JAMA 1995;273:1429–1435

381. McCrindle BW, Ose L, Marais AD. Effi-cacy and safety of atorvastatin in chil-dren and adolescents with familialhypercholesterolemia or severe hyper-lipidemia: a multicenter, randomized,placebo-controlled trial. J Pediatr 2003;143:74–80

382. de Jongh S, Lilien MR, op’t Roodt J,Stroes ES, Bakker HD, Kastelein JJ; de JS.Early statin therapy restores endothelialfunction in children with familial hy-percholesterolemia. J Am Coll Cardiol2002;40:2117–2121

383. WiegmanA,Hutten BA, de Groot E, et al.Efficacy and safety of statin therapy inchildren with familial hypercholesterol-emia: a randomized controlled trial.JAMA 2004;292:331–337

384. Cho YH, Craig ME, Hing S, Gallego PH,Poon M, Chan A, Donaghue KC: Mi-crovascular complications assessment inadolescents with 2- to 5-yr duration oftype 1 diabetes from 1990 to 2006. Pe-diatr Diabetes. 24 March 2011 [Epubahead of print]

385. Holmes GK. Screening for coeliac dis-ease in type 1 diabetes. Arch Dis Child2002;87:495–498

386. Rewers M, Liu E, Simmons J, RedondoMJ, Hoffenberg EJ: Celiac disease asso-ciated with type 1 diabetes mellitus.Endocrinol Metab Clin North Am 2004;33:197–214

387. Kurppa K, Ashorn M, Iltanen S, KoskinenLL, Saavalainen P, Koskinen O, Maki M,KaukinenK: Celiac disease without villousatrophy in children: a prospective study.J Pediatr 2010157:373–380

388. Abid N, McGlone O, Cardwell C,McCallion W, Carson D. Clinical andmetabolic effects of gluten free diet inchildren with type 1 diabetes and coeliacdisease. Pediatr Diabetes 2011;12:322–325

389. Roldán MB, Alonso M, Barrio R. Thyroidautoimmunity in children and adoles-cents with Type 1 diabetes mellitus. Di-abetes Nutr Metab 1999;12:27–31


Position Statement

390. Triolo TM, Armstrong TK, McFann K,et al. Additional autoimmune diseasefound in 33% of patients at type 1 di-abetes onset. Diabetes Care 2011;34:1211–1213

391. Kordonouri O, Deiss D, Danne T, DorowA, Bassir C, Grüters-Kieslich A. Pre-dictivity of thyroid autoantibodies forthe development of thyroid disorders inchildren and adolescents with Type 1diabetes. Diabet Med 2002;19:518–521

392. Mohn A, Di Michele S, Di Luzio R,Tumini S, Chiarelli F. The effect of sub-clinical hypothyroidism on metaboliccontrol in children and adolescents withType 1 diabetes mellitus. Diabet Med2002;19:70–73

393. Chase HP, Garg SK, Cockerham RS,Wilcox WD, Walravens PA. Thyroidhormone replacement and growth ofchildren with subclinical hypothyroid-ism and diabetes. Diabet Med 1990;7:299–303

394. American Diabetes Association. Diabetescare in the school and day care setting.Diabetes Care 2010;33(Suppl 1):S70–S74

395. Arnett JJ. Emerging adulthood. A theoryof development from the late teensthrough the twenties. Am Psychol 2000;55:469–480

396. Weissberg-Benchell J, Wolpert H,Anderson BJ. Transitioning from pedi-atric to adult care: a new approach tothe post-adolescent young person withtype 1 diabetes. Diabetes Care 2007;30:2441–2446

397. American Diabetes Association. Transi-tion in care from youth to adulthood.Diabetes Care. 2011;34:2477–2485

398. Bryden KS, Peveler RC, Stein A, Neil A,Mayou RA, Dunger DB. Clinical andpsychological course of diabetes fromadolescence to young adulthood: a lon-gitudinal cohort study. Diabetes Care2001;24:1536–1540

399. Laing SP, Jones ME, Swerdlow AJ,Burden AC, GatlingW. Psychosocial andsocioeconomic risk factors for prematuredeath in young people with type 1 di-abetes.DiabetesCare 2005;28:1618–1623

400. Eppens MC, Craig ME, Cusumano J,et al. Prevalence of diabetes complica-tions in adolescents with type 2 com-pared with type 1 diabetes. DiabetesCare 2006;29:1300–1306

401. Hattersley A, Bruining J, Shield J,Njolstad P, Donaghue KC. The diagnosisand management of monogenic diabetesin children and adolescents. Pediatr Di-abetes 2009;10(Suppl 12):33–42

402. Cooper WO, Hernandez-Diaz S,Arbogast PG, et al. Major congenitalmalformations after first-trimester ex-posure to ACE inhibitors. N Engl J Med2006;354:2443–2451

403. American Diabetes Association. Pre-conception care of women with diabetes.Diabetes Care 2004;27(Suppl 1):S76–S78

404. Brown AF, Mangione CM, Saliba D,Sarkisian CA; California HealthcareFoundation/American Geriatrics SocietyPanel on Improving Care for Elders withDiabetes. Guidelines for improving thecare of the older person with diabetesmellitus. J Am Geriatr Soc 2003;51(Suppl Guidelines):S265–S280

405. Curb JD, Pressel SL, Cutler JA, et al.;Systolic Hypertension in the ElderlyProgram Cooperative Research Group.Effect of diuretic-based antihypertensivetreatment on cardiovascular disease riskin older diabetic patients with isolatedsystolic hypertension. JAMA 1996;276:1886–1892

406. Beckett NS, Peters R, Fletcher AE, et al.;HYVET Study Group. Treatment of hy-pertension in patients 80 years of age orolder. N Engl J Med 2008;358:1887–1898

407. Moran A, Dunitz J, Nathan B, Saeed A,Holme B, Thomas W. Cystic fibrosis-related diabetes: current trends in preva-lence, incidence, and mortality. DiabetesCare 2009;32:1626–1631

408. Moran A, Brunzell C, Cohen RC, et al.;CFRD Guidelines Committee. Clinicalcare guidelines for cystic fibrosis-relateddiabetes: a position statement of theAmerican Diabetes Association and aclinical practice guideline of the CysticFibrosis Foundation, endorsed by thePediatric Endocrine Society. DiabetesCare 2010;33:2697–2708

409. Clement S, Braithwaite SS, Magee MF,et al.; American Diabetes Association;Diabetes in Hospitals Writing Commit-tee. Management of diabetes and hy-perglycemia in hospitals. Diabetes Care2004;27:553–591

410. Moghissi ES, Korytkowski MT, DiNardoM, et al.; American Association of ClinicalEndocrinologists; American DiabetesAssociation. American Association ofClinical Endocrinologists and AmericanDiabetes Association consensus statementon inpatient glycemic control. DiabetesCare 2009;32:1119–1131

411. van den Berghe G, Wouters P, WeekersF, et al. Intensive insulin therapy in thecritically ill patients. N Engl J Med 2001;345:1359–1367

412. Malmberg K, Norhammar A, Wedel H,Rydén L. Glycometabolic state at ad-mission: important risk marker of mor-tality in conventionally treated patientswith diabetes mellitus and acute myo-cardial infarction: long-term results fromthe Diabetes and Insulin-Glucose In-fusion in Acute Myocardial Infarction(DIGAMI) study. Circulation 1999;99:2626–2632

413. Wiener RS, Wiener DC, Larson RJ.Benefits and risks of tight glucose controlin critically ill adults: a meta-analysis.JAMA 2008;300:933–944

414. Brunkhorst FM, Engel C, Bloos F, et al.;German Competence Network Sepsis

(SepNet). Intensive insulin therapy andpentastarch resuscitation in severe sep-sis. N Engl J Med 2008;358:125–139

415. Finfer S, Chittock DR, Su SY, et al.; NICE-SUGAR Study Investigators. Intensiveversus conventional glucose control incritically ill patients. N Engl J Med 2009;360:1283–1297

416. Krinsley JS, Grover A. Severe hypogly-cemia in critically ill patients: risk factorsand outcomes. Crit Care Med 2007;35:2262–2267

417. Van den Berghe G, Wilmer A, HermansG, et al. Intensive insulin therapy in themedical ICU. N Engl J Med 2006;354:449–461

418. Griesdale DE, de Souza RJ, van Dam RM,et al. Intensive insulin therapy andmortality among critically ill patients:a meta-analysis including NICE-SUGARstudy data. CMAJ 2009;180:821–827

419. Saudek CD, Herman WH, Sacks DB,Bergenstal RM, Edelman D, DavidsonMB. A new look at screening and di-agnosing diabetes mellitus. J Clin En-docrinol Metab 2008;93:2447–2453

420. Cryer PE, Davis SN, Shamoon H. Hy-poglycemia in diabetes. Diabetes Care2003;26:1902–1912

421. Bernard JB, Munoz C, Harper J, MurielloM, Rico E, Baldwin D. Treatment of in-patient hyperglycemia beginning in theemergency department: a randomizedtrial using insulins aspart and detemircompared with usual care. J Hosp Med2011;6:279–284

422. Czosnowski QA, Swanson JM, Lobo BL,Broyles JE, Deaton PR, Finch CK. Eval-uation of glycemic control followingdiscontinuation of an intensive insulinprotocol. J Hosp Med 2009;4:28–34

423. Shomali MI, Herr DL, Hill PC,Pehlivanova M, Sharretts JM, Magee MF.Transition to target: a prospective ran-domized trial comparing three formulaefor determination of subcutaneous basalinsulin dosing at the time of transitionfrom intravenous insulin therapy follow-ing cardiac surgery. Diabetes TechnolTher 2011;13:121–126

424. Umpierrez GE, Smiley D, Jacobs S, et al.Randomized study of basal-bolus insulintherapy in the inpatient management ofpatients with type 2 diabetes undergoinggeneral surgery (RABBIT 2 surgery). Di-abetes Care 2011;34:256–261

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Position Statement

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Position Statement

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Position Statement

Diagnosis and Classification of DiabetesMellitusAMERICAN DIABETES ASSOCIATION

DEFINITION ANDDESCRIPTION OF DIABETESMELLITUSdDiabetes is a group ofmetabolic diseases characterized by hy-perglycemia resulting from defects in in-sulin secretion, insulin action, or both.The chronic hyperglycemia of diabetes isassociated with long-term damage, dys-function, and failure of different organs,especially the eyes, kidneys, nerves, heart,and blood vessels.

Several pathogenic processes are in-volved in the development of diabetes.These range from autoimmune destruc-tion of the b-cells of the pancreas withconsequent insulin deficiency to abnor-malities that result in resistance to insulinaction. The basis of the abnormalities incarbohydrate, fat, and protein metabo-lism in diabetes is deficient action of in-sulin on target tissues. Deficient insulinaction results from inadequate insulin se-cretion and/or diminished tissue respon-ses to insulin at one or more points in thecomplex pathways of hormone action.Impairment of insulin secretion and de-fects in insulin action frequently coexist inthe same patient, and it is often unclearwhich abnormality, if either alone, is theprimary cause of the hyperglycemia.

Symptoms ofmarked hyperglycemia in-cludepolyuria,polydipsia,weight loss,some-times with polyphagia, and blurred vision.Impairment of growth and susceptibility tocertain infections may also accompanychronic hyperglycemia. Acute, life-threaten-ing consequences of uncontrolled diabetesare hyperglycemia with ketoacidosis or thenonketotic hyperosmolar syndrome.

Long-term complications of diabetesinclude retinopathy with potential lossof vision; nephropathy leading to renalfailure; peripheral neuropathy with riskof foot ulcers, amputations, and Charcotjoints; and autonomic neuropathy caus-ing gastrointestinal, genitourinary, and

cardiovascular symptoms and sexual dys-function. Patients with diabetes have anincreased incidence of atherosclerotic car-diovascular, peripheral arterial, and cere-brovascular disease. Hypertension andabnormalities of lipoprotein metabolismare often found in people with diabetes.

The vast majority of cases of diabetesfall into two broad etiopathogenetic cate-gories (discussed in greater detail below).In one category, type 1 diabetes, the causeis an absolute deficiency of insulin secre-tion. Individuals at increased risk of de-veloping this type of diabetes can often beidentified by serological evidence of anautoimmune pathologic process occurringin the pancreatic islets and by geneticmarkers. In the other, much more preva-lent category, type 2 diabetes, the cause is acombination of resistance to insulin actionand an inadequate compensatory insulinsecretory response. In the latter category, adegree of hyperglycemia sufficient to causepathologic and functional changes in var-ious target tissues, but without clinicalsymptoms, may be present for a longperiod of time before diabetes is detected.During this asymptomatic period, it ispossible to demonstrate an abnormality incarbohydrate metabolism by measurementof plasma glucose in the fasting state orafter a challenge with an oral glucose load.

The degree of hyperglycemia (if any)may change over time, depending on theextent of the underlying disease process(Fig. 1). A disease process may be presentbut may not have progressed far enoughto cause hyperglycemia. The same diseaseprocess can cause impaired fasting glu-cose (IFG) and/or impaired glucose toler-ance (IGT) without fulfilling the criteriafor the diagnosis of diabetes. In some in-dividuals with diabetes, adequate glyce-mic control can be achieved with weightreduction, exercise, and/or oral glucose-lowering agents. These individuals

therefore do not require insulin. Otherindividuals who have some residual insu-lin secretion but require exogenous insu-lin for adequate glycemic control cansurvive without it. Individuals with ex-tensive b-cell destruction and thereforeno residual insulin secretion require in-sulin for survival. The severity of the met-abolic abnormality can progress, regress,or stay the same. Thus, the degree of hy-perglycemia reflects the severity of theunderlying metabolic process and itstreatment more than the nature of theprocess itself.

CLASSIFICATION OFDIABETES MELLITUS ANDOTHER CATEGORIESOF GLUCOSEREGULATIONdAssigning a type ofdiabetes to an individual often dependson the circumstances present at the timeof diagnosis, and many diabetic individ-uals do not easily fit into a single class. Forexample, a person with gestational di-abetes mellitus (GDM) may continue tobe hyperglycemic after delivery and maybe determined to have, in fact, type 2diabetes. Alternatively, a person whoacquires diabetes because of large dosesof exogenous steroids may become nor-moglycemic once the glucocorticoids arediscontinued, but then may develop di-abetes many years later after recurrentepisodes of pancreatitis. Another examplewould be a person treated with thiazideswho develops diabetes years later. Becausethiazides in themselves seldomcause severehyperglycemia, such individuals probablyhave type 2 diabetes that is exacerbated bythe drug. Thus, for the clinician andpatient,it is less important to label the particulartype of diabetes than it is to understand thepathogenesis of the hyperglycemia and totreat it effectively.

Type 1 diabetes (b-cell destruction,usually leading to absolute insulindeficiency)Immune-mediated diabetes. This formof diabetes, which accounts for only5–10% of those with diabetes, previouslyencompassed by the terms insulin-dependent diabetes, type 1 diabetes, orjuvenile-onset diabetes, results from a cel-lular-mediated autoimmune destruction


Section on gestational diabetes diagnosis revised Fall 2010.DOI: 10.2337/dc12-s064© 2012 by the American Diabetes Association. Readers may use this article as long as the work is properly




of the b-cells of the pancreas. Markers ofthe immune destruction of the b-cell in-clude islet cell autoantibodies, autoanti-bodies to insulin, autoantibodies to GAD(GAD65), and autoantibodies to the ty-rosine phosphatases IA-2 and IA-2b.One and usually more of these autoanti-bodies are present in 85–90% of individ-uals when fasting hyperglycemia isinitially detected. Also, the disease hasstrong HLA associations, with linkage tothe DQA and DQB genes, and it is influ-enced by the DRB genes. These HLA-DR/DQ alleles can be either predisposing orprotective.

In this form of diabetes, the rate ofb-cell destruction is quite variable, beingrapid in some individuals (mainly infantsand children) and slow in others (mainlyadults). Some patients, particularly chil-dren and adolescents, may present withketoacidosis as the first manifestation ofthe disease. Others have modest fastinghyperglycemia that can rapidly changeto severe hyperglycemia and/or ketoaci-dosis in the presence of infection or otherstress. Still others, particularly adults,may retain residual b-cell function suffi-cient to prevent ketoacidosis for manyyears; such individuals eventually be-come dependent on insulin for survivaland are at risk for ketoacidosis. At thislatter stage of the disease, there is littleor no insulin secretion, as manifested bylow or undetectable levels of plasma

C-peptide. Immune-mediated diabetescommonly occurs in childhood and ado-lescence, but it can occur at any age, evenin the 8th and 9th decades of life.

Autoimmune destruction of b-cellshas multiple genetic predispositions andis also related to environmental factorsthat are still poorly defined. Although pa-tients are rarely obese when they presentwith this type of diabetes, the presence ofobesity is not incompatible with the diag-nosis. These patients are also prone toother autoimmune disorders such asGraves’ disease, Hashimoto’s thyroiditis,Addison’s disease, vitiligo, celiac sprue,autoimmune hepatitis, myasthenia gravis,and pernicious anemia.Idiopathic diabetes. Some forms of type1 diabetes have no known etiologies.Some of these patients have permanentinsulinopenia and are prone to ketoaci-dosis, but have no evidence of autoim-munity. Although only a minority ofpatients with type 1 diabetes fall intothis category, of those who do, most are ofAfrican or Asian ancestry. Individualswith this form of diabetes suffer fromepisodic ketoacidosis and exhibit varyingdegrees of insulin deficiency betweenepisodes. This form of diabetes is stronglyinherited, lacks immunological evidencefor b-cell autoimmunity, and is not HLAassociated. An absolute requirement forinsulin replacement therapy in affectedpatients may come and go.

Type 2 diabetes (ranging frompredominantly insulin resistancewith relative insulin deficiency topredominantly an insulin secretorydefect with insulin resistance)This form of diabetes, which accounts for;90–95% of those with diabetes, previ-ously referred to as non–insulin-depen-dent diabetes, type 2 diabetes, or adult-onset diabetes, encompasses individualswho have insulin resistance and usuallyhave relative (rather than absolute) insu-lin deficiency At least initially, and oftenthroughout their lifetime, these individu-als do not need insulin treatment to sur-vive. There are probably many differentcauses of this form of diabetes. Althoughthe specific etiologies are not known, au-toimmune destruction of b-cells does notoccur, and patients do not have any of theother causes of diabetes listed above orbelow.

Most patients with this form of di-abetes are obese, and obesity itself causessome degree of insulin resistance. Patientswho are not obese by traditional weightcriteria may have an increased percentageof body fat distributed predominantly inthe abdominal region. Ketoacidosis sel-dom occurs spontaneously in this type ofdiabetes; when seen, it usually arises inassociation with the stress of anotherillness such as infection. This form ofdiabetes frequently goes undiagnosed formany years because the hyperglycemia

Figure 1dDisorders of glycemia: etiologic types and stages. *Even after presenting in ketoacidosis, these patients can briefly return to normo-glycemia without requiring continuous therapy (i.e., “honeymoon” remission); **in rare instances, patients in these categories (e.g., Vacor toxicity,type 1 diabetes presenting in pregnancy) may require insulin for survival.


Position Statement

develops gradually and at earlier stages isoften not severe enough for the patient tonotice any of the classic symptoms ofdiabetes. Nevertheless, such patients areat increased risk of developing macro-vascular and microvascular complica-tions. Whereas patients with this form ofdiabetes may have insulin levels thatappear normal or elevated, the higherblood glucose levels in these diabeticpatients would be expected to result ineven higher insulin values had their b-cellfunction been normal. Thus, insulin se-cretion is defective in these patients andinsufficient to compensate for insulin re-sistance. Insulin resistance may improvewith weight reduction and/or pharmaco-logical treatment of hyperglycemia but isseldom restored to normal. The risk ofdeveloping this form of diabetes increaseswith age, obesity, and lack of physical ac-tivity. It occurs more frequently in womenwith prior GDM and in individuals withhypertension or dyslipidemia, and its fre-quency varies in different racial/ethnic sub-groups. It is often associated with a stronggenetic predisposition, more so than is theautoimmune form of type 1 diabetes. How-ever, the genetics of this form of diabetesare complex and not clearly defined.

Other specific types of diabetesGenetic defects of the b-cell. Severalforms of diabetes are associated withmonogenetic defects in b-cell function.These forms of diabetes are frequentlycharacterized by onset of hyperglycemiaat an early age (generally before age 25years). They are referred to as maturity-onset diabetes of the young (MODY) andare characterized by impaired insulin se-cretion with minimal or no defects in in-sulin action. They are inherited in anautosomal dominant pattern. Abnormali-ties at six genetic loci on different chro-mosomes have been identified to date.The most common form is associatedwith mutations on chromosome 12 in ahepatic transcription factor referred to ashepatocyte nuclear factor (HNF)-1a. Asecond form is associated with mutationsin the glucokinase gene on chromosome7p and results in a defective glucokinasemolecule. Glucokinase converts glucoseto glucose-6-phosphate, the metabolismof which, in turn, stimulates insulin secre-tion by the b-cell. Thus, glucokinaseserves as the “glucose sensor” for theb-cell. Because of defects in the glucoki-nase gene, increased plasma levels of glu-cose are necessary to elicit normal levelsof insulin secretion. The less common

forms result frommutations in other tran-scription factors, including HNF-4a,HNF-1b, insulin promoter factor (IPF)-1, and NeuroD1.

Point mutations in mitochondrialDNA have been found to be associatedwith diabetes and deafness The mostcommon mutation occurs at position3,243 in the tRNA leucine gene, leadingto an A-to-G transition. An identicallesion occurs in the MELAS syndrome(mitochondrial myopathy, encephalopa-thy, lactic acidosis, and stroke-like syn-drome); however, diabetes is not part ofthis syndrome, suggesting different phe-notypic expressions of this genetic lesion.

Genetic abnormalities that result inthe inability to convert proinsulin to in-sulin have been identified in a few fami-lies, and such traits are inherited in anautosomal dominant pattern. The resul-tant glucose intolerance is mild. Similarly,the production of mutant insulin mole-cules with resultant impaired receptorbinding has also been identified in a fewfamilies and is associated with an autoso-mal inheritance and only mildly impairedor even normal glucose metabolism.Genetic defects in insulin action. Thereare unusual causes of diabetes that resultfrom genetically determined abnormali-ties of insulin action. The metabolic ab-normalities associated with mutations ofthe insulin receptor may range fromhyperinsulinemia and modest hyperglyce-mia to severe diabetes. Some individualswith these mutations may have acanthosisnigricans. Women may be virilized andhave enlarged, cystic ovaries. In the past,this syndrome was termed type A insulinresistance. Leprechaunism and the Rabson-Mendenhall syndrome are two pediatricsyndromes that have mutations in theinsulin receptor gene with subsequentalterations in insulin receptor functionand extreme insulin resistance. The formerhas characteristic facial features and isusually fatal in infancy, while the latter isassociated with abnormalities of teeth andnails and pineal gland hyperplasia.

Alterations in the structure and func-tion of the insulin receptor cannot bedemonstrated in patients with insulin-resistant lipoatrophic diabetes. Therefore,it is assumed that the lesion(s) must residein the postreceptor signal transductionpathways.Diseases of the exocrine pancreas. Anyprocess that diffusely injures the pancreascan cause diabetes. Acquired processesinclude pancreatitis, trauma, infection, pan-createctomy, and pancreatic carcinoma.

With the exception of that caused bycancer, damage to the pancreas must beextensive for diabetes to occur; adreno-carcinomas that involve only a smallportion of the pancreas have been associ-ated with diabetes. This implies a mech-anism other than simple reduction inb-cell mass. If extensive enough, cystic fi-brosis and hemochromatosis will alsodamage b-cells and impair insulin secre-tion. Fibrocalculous pancreatopathy maybe accompanied by abdominal pain radi-ating to the back and pancreatic calcifica-tions identified on X-ray examination.Pancreatic fibrosis and calcium stonesin the exocrine ducts have been found atautopsy.Endocrinopathies. Several hormones(e.g., growth hormone, cortisol, gluca-gon, epinephrine) antagonize insulin ac-tion. Excess amounts of these hormones(e.g., acromegaly, Cushing’s syndrome,glucagonoma, pheochromocytoma, re-spectively) can cause diabetes. This gen-erally occurs in individuals withpreexisting defects in insulin secretion,and hyperglycemia typically resolveswhen the hormone excess is resolved.

Somatostatinoma- and aldostero-noma-induced hypokalemia can causediabetes, at least in part, by inhibitinginsulin secretion. Hyperglycemia gener-ally resolves after successful removal ofthe tumor.Drug- or chemical-induced diabetes.Many drugs can impair insulin secretion.These drugs may not cause diabetes bythemselves, but they may precipitate di-abetes in individuals with insulin resis-tance. In such cases, the classification isunclear because the sequence or relativeimportance of b-cell dysfunction and in-sulin resistance is unknown. Certain tox-ins such as Vacor (a rat poison) andintravenous pentamidine can perma-nently destroy pancreatic b-cells. Suchdrug reactions fortunately are rare. Thereare also many drugs and hormones thatcan impair insulin action. Examples in-clude nicotinic acid and glucocorticoids.Patients receiving a-interferon have beenreported to develop diabetes associatedwith islet cell antibodies and, in certaininstances, severe insulin deficiency. Thelist shown in Table 1 is not all-inclusive,but reflects the more commonly recog-nized drug-, hormone-, or toxin-inducedforms of diabetes.Infections. Certain viruses have beenassociated with b-cell destruction. Diabe-tes occurs in patients with congenital ru-bella, although most of these patients


Diagnosis and Classification

have HLA and immune markers charac-teristic of type 1 diabetes. In addition,coxsackievirus B, cytomegalovirus, ade-novirus, and mumps have been impli-cated in inducing certain cases of thedisease.Uncommon forms of immune-mediateddiabetes. In this category, there are twoknown conditions, and others are likelyto occur. The stiff-man syndrome is anautoimmune disorder of the central ner-vous system characterized by stiffness ofthe axial muscles with painful spasms.Patients usually have high titers of theGAD autoantibodies, and approximatelyone-third will develop diabetes.

Anti-insulin receptor antibodies cancause diabetes by binding to the insulinreceptor, thereby blocking the binding ofinsulin to its receptor in target tissues.However, in some cases, these antibodiescan act as an insulin agonist after bindingto the receptor and can thereby causehypoglycemia. Anti-insulin receptor anti-bodies are occasionally found in patientswith systemic lupus erythematosus andother autoimmune diseases. As in otherstates of extreme insulin resistance, pa-tients with anti-insulin receptor antibod-ies often have acanthosis nigricans. In thepast, this syndrome was termed type Binsulin resistance.Other genetic syndromes sometimesassociated with diabetes. Many geneticsyndromes are accompanied by an in-creased incidence of diabetes. These in-clude the chromosomal abnormalities ofDown syndrome, Klinefelter syndrome,and Turner syndrome. Wolfram’s syn-drome is an autosomal recessive disordercharacterized by insulin-deficient diabe-tes and the absence of b-cells at autopsy.Additional manifestations include diabetesinsipidus, hypogonadism, optic atrophy,and neural deafness. Other syndromes arelisted in Table 1.

Gestational diabetes mellitusFor many years, GDM has been defined asany degree of glucose intolerance withonset or first recognition during preg-nancy. Although most cases resolve withdelivery, the definition applied whetheror not the condition persisted after preg-nancy and did not exclude the possibilitythat unrecognized glucose intolerancemay have antedated or begun concomi-tantly with the pregnancy. This definitionfacilitated a uniform strategy for detectionand classification of GDM, but its limi-tations were recognized for many years.As the ongoing epidemic of obesity and

Table 1dEtiologic classification of diabetes mellitus

I. Type 1 diabetes (b-cell destruction, usually leading to absolute insulin deficiency)A. Immune mediatedB. Idiopathic

II. Type 2 diabetes (may range from predominantly insulin resistance with relative insulin deficiencyto a predominantly secretory defect with insulin resistance)

III. Other specific typesA. Genetic defects of b-cell function

1. Chromosome 12, HNF-1a (MODY3)2. Chromosome 7, glucokinase (MODY2)3. Chromosome 20, HNF-4a (MODY1)4. Chromosome 13, insulin promoter factor-1 (IPF-1; MODY4)5. Chromosome 17, HNF-1b (MODY5)6. Chromosome 2, NeuroD1 (MODY6)7. Mitochondrial DNA8. Others

B. Genetic defects in insulin action1. Type A insulin resistance2. Leprechaunism3. Rabson-Mendenhall syndrome4. Lipoatrophic diabetes5. Others

C. Diseases of the exocrine pancreas1. Pancreatitis2. Trauma/pancreatectomy3. Neoplasia4. Cystic fibrosis5. Hemochromatosis6. Fibrocalculous pancreatopathy7. Others

D. Endocrinopathies1. Acromegaly2. Cushing’s syndrome3. Glucagonoma4. Pheochromocytoma5. Hyperthyroidism6. Somatostatinoma7. Aldosteronoma8. Others

E. Drug or chemical induced1. Vacor2. Pentamidine3. Nicotinic acid4. Glucocorticoids5. Thyroid hormone6. Diazoxide7. b-adrenergic agonists8. Thiazides9. Dilantin

10. g-Interferon11. Others

F. Infections1. Congenital rubella2. Cytomegalovirus3. Others

G. Uncommon forms of immune-mediated diabetes1. “Stiff-man” syndrome2. Anti-insulin receptor antibodies3. Others

H. Other genetic syndromes sometimes associated with diabetes1. Down syndrome2. Klinefelter syndrome3. Turner syndrome4. Wolfram syndrome5. Friedreich ataxia6. Huntington chorea7. Laurence-Moon-Biedl syndrome8. Myotonic dystrophy9. Porphyria

10. Prader-Willi syndrome11. Others

IV. Gestational diabetes mellitus

Patients with any form of diabetes may require insulin treatment at some stage of their disease. Such use ofinsulin does not, of itself, classify the patient.


Position Statement

diabetes has led to more type 2 diabetes inwomen of childbearing age, the number ofpregnant womenwith undiagnosed type 2diabetes has increased.

After deliberations in 2008–2009, theInternational Association of Diabetes andPregnancy Study Groups (IADPSG), aninternational consensus group with rep-resentatives from multiple obstetrical anddiabetes organizations, including theAmerican Diabetes Association (ADA),recommended that high-risk womenfound to have diabetes at their initial pre-natal visit, using standard criteria (Table3), receive a diagnosis of overt, not gesta-tional, diabetes. Approximately 7% of allpregnancies (ranging from 1 to 14%, de-pending on the population studied andthe diagnostic tests employed) are com-plicated by GDM, resulting in more than200,000 cases annually.

CATEGORIES OF INCREASEDRISK FOR DIABETESdIn 1997 and2003, The Expert Committee on Diagno-sis and Classification of Diabetes Mellitus(1,2) recognized an intermediate group ofindividuals whose glucose levels do notmeet criteria for diabetes, yet are higherthan those considered normal. These peo-ple were defined as having impaired fast-ing glucose (IFG) [fasting plasma glucose(FPG) levels 100 mg/dl (5.6 mmol/l) to125mg/dl (6.9 mmol/l)], or impaired glu-cose tolerance (IGT) [2-h values in theoral glucose tolerance test (OGTT) of140 mg/dl (7.8 mmol/l) to 199 mg/dl(11.0 mmol/l)].

Individuals with IFG and/or IGT havebeen referred to as having pre-diabetes,indicating the relatively high risk for thefuture development of diabetes. IFG andIGT should not be viewed as clinicalentities in their own right but rather riskfactors for diabetes as well as cardiovas-cular disease. They can be observed asintermediate stages in any of the diseaseprocesses listed in Table 1. IFG and IGTare associated with obesity (especially

abdominal or visceral obesity), dyslipide-mia with high triglycerides and/or lowHDL cholesterol, and hypertension.Structured lifestyle intervention, aimedat increasing physical activity and pro-ducing 5–10% loss of body weight, andcertain pharmacological agents have beendemonstrated to prevent or delay the de-velopment of diabetes in people with IGT;the potential impact of such interventionsto reduce mortality or the incidence ofcardiovascular disease has not been dem-onstrated to date. It should be noted thatthe 2003 ADA Expert Committee reportreduced the lower FPG cut point to defineIFG from 110 mg/dl (6.1 mmol/l) to 100mg/dl (5.6 mmol/l), in part to ensure thatprevalence of IFG was similar to that ofIGT. However, the World Health Organi-zation (WHO) and many other diabetesorganizations did not adopt this change inthe definition of IFG.

As A1C is used more commonly todiagnose diabetes in individuals with riskfactors, it will also identify those at higherrisk for developing diabetes in the future.When recommending the use of the A1Cto diagnose diabetes in its 2009 report,the International Expert Committee (3)stressed the continuum of risk for diabe-tes with all glycemicmeasures and did notformally identify an equivalent intermedi-ate category for A1C. The group did notethat those with A1C levels above the lab-oratory “normal” range but below the di-agnostic cut point for diabetes (6.0 to,6.5%) are at very high risk of develop-ing diabetes. Indeed, incidence of diabe-tes in people with A1C levels in this rangeis more than 10 times that of people withlower levels (4–7). However, the 6.0 to,6.5% range fails to identify a substantialnumber of patients who have IFG and/orIGT. Prospective studies indicate thatpeople within the A1C range of 5.5–6.0% have a 5-year cumulative incidenceof diabetes that ranges from 12 to 25%(4–7), which is appreciably (three- toeightfold) higher than incidence in theU.S. population as a whole (8). Analysesof nationally representative data from theNational Health and Nutrition Examina-tion Survey (NHANES) indicate that theA1C value that most accurately identifiespeople with IFG or IGT falls between 5.5and 6.0%. In addition, linear regressionanalyses of these data indicate that amongthe nondiabetic adult population, an FPGof 110 mg/dl (6.1 mmol/l) correspondsto an A1C of 5.6%, while an FPG of 100mg/dl (5.6 mmol/l) corresponds to anA1C of 5.4% (R.T. Ackerman, personal

communication). Finally, evidence fromthe Diabetes Prevention Program (DPP),wherein the mean A1C was 5.9% (SD0.5%), indicates that preventive interven-tions are effective in groups of people withA1C levels both below and above 5.9%(9). For these reasons, the most appropri-ate A1C level above which to initiate pre-ventive interventions is likely to besomewhere in the range of 5.5–6%.

As was the case with FPG and 2-h PG,defining a lower limit of an intermediatecategory of A1C is somewhat arbitrary,as the risk of diabetes with any measureor surrogate of glycemia is a continuum,extending well into the normal ranges. Tomaximize equity and efficiency of pre-ventive interventions, such an A1C cutpoint should balance the costs of “falsenegatives” (failing to identify those whoare going to develop diabetes) againstthe costs of “false positives” (falsely iden-tifying and then spending intervention re-sources on those who were not going todevelop diabetes anyway).

Compared to the fasting glucose cut-point of 100 mg/dl (5.6 mmol/l), an A1Ccutpoint of 5.7% is less sensitive but morespecific and has a higher positive predic-tive value to identify people at risk forlater development of diabetes. A largeprospective study found that a 5.7% cut-point has a sensitivity of 66% and speci-ficity of 88% for the identification ofsubsequent 6-year diabetes incidence(10). Receiver operating curve analysesof nationally representative U.S. data(NHANES 1999-2006) indicate that anA1C value of 5.7% has modest sensitivity(39-45%) but high specificity (81-91%)to identify cases of IFP (FPG .100 mg/dl) (5.6 mmol/l) or IGT (2-h glucose .140 mg/dl) (R.T. Ackerman, personalcommunication). Other analyses suggestthat an A1C of 5.7% is associated withdiabetes risk similar to the high-risk par-ticipants in the DPP (R.T. Ackerman, per-sonal communication). Hence, it isreasonable to consider an A1C range of5.7 to 6.4% as identifying individualswith high risk for future diabetes and towhom the term pre-diabetes may be ap-plied if desired.

Individuals with an A1C of 5.7–6.4%should be informed of their increased riskfor diabetes as well as cardiovascular dis-ease and counseled about effective strate-gies, such as weight loss and physicalactivity, to lower their risks. As with glu-cose measurements, the continuum of riskis curvilinear, so that as A1C rises, the riskof diabetes rises disproportionately.

Table 2dCategories of increased risk fordiabetes*

FPG 100mg/dl (5.6 mmol/l) to 125 mg/dl (6.9mmol/l) [IFG]

2-h PG in the 75-g OGTT 140 mg/dl (7.8mmol/l) to 199 mg/dl (11.0 mmol/l) [IGT]

A1C 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.



Accordingly, interventions should bemost intensive and follow-up should beparticularly vigilant for those with A1Clevels above 6.0%, who should be consid-ered to be at very high risk. However, justas an individual with a fasting glucose of98 mg/dl (5.4 mmol/l) may not be at neg-ligible risk for diabetes, individuals withA1C levels below 5.7% may still be atrisk, depending on level of A1C and pres-ence of other risk factors, such as obesityand family history.

Table 2 summarizes the categories ofincreased risk for diabetes. Evaluation ofpatients at risk should incorporate aglobal risk factor assessment for both di-abetes and cardiovascular disease. Screen-ing for and counseling about risk ofdiabetes should always be in the prag-matic context of the patient’s comorbidi-ties, life expectancy, personal capacity toengage in lifestyle change, and overallhealth goals.

DIAGNOSTIC CRITERIA FORDIABETES MELLITUSdFor deca-des, the diagnosis of diabetes has beenbased on glucose criteria, either the FPGor the 75-g OGTT. In 1997, the firstExpert Committee on the Diagnosis andClassification of Diabetes Mellitus revisedthe diagnostic criteria, using the observedassociation between FPG levels and pres-ence of retinopathy as the key factor withwhich to identify threshold glucose level.The Committee examined data from threecross-sectional epidemiologic studies thatassessed retinopathy with fundus pho-tography or direct ophthalmoscopy andmeasured glycemia as FPG, 2-h PG, andA1C. These studies demonstrated glyce-mic levels below which there was littleprevalent retinopathy and above whichthe prevalence of retinopathy increased inan apparently linear fashion. The decilesof the three measures at which retinopa-thy began to increase were the same foreach measure within each population.Moreover, the glycemic values abovewhich retinopathy increased were similaramong the populations. These analyseshelped to inform a new diagnostic cutpoint of $126 mg/dl (7.0 mmol/l) forFPG and confirmed the long-standing di-agnostic 2-h PG value of $200 mg/dl(11.1 mmol/l).

A1C is a widely used marker ofchronic glycemia, reflecting averageblood glucose levels over a 2- to 3-monthperiod of time. The test plays a critical rolein the management of the patient withdiabetes, since it correlates well with both

microvascular and, to a lesser extent,macrovascular complications and iswidely used as the standard biomarkerfor the adequacy of glycemic manage-ment. Prior Expert Committees have notrecommended use of the A1C for diag-nosis of diabetes, in part due to lack ofstandardization of the assay. However,A1C assays are now highly standardizedso that their results can be uniformlyapplied both temporally and across pop-ulations. In their recent report (3), an In-ternational Expert Committee, after anextensive review of both established andemerging epidemiological evidence, rec-ommended the use of the A1C test to di-agnose diabetes, with a threshold of$6.5%, and ADA affirms this decision.The diagnostic A1C cut point of 6.5% isassociated with an inflection point for ret-inopathy prevalence, as are the diagnosticthresholds for FPG and 2-h PG (3). Thediagnostic test should be performedusing a method that is certified by the Na-tional Glycohemoglobin StandardizationProgram (NGSP) and standardized ortraceable to the Diabetes Control andComplications Trial reference assay.Point-of-care A1C assays are not suffi-ciently accurate at this time to use for di-agnostic purposes.

There is an inherent logic to using amore chronic versus an acute marker ofdysglycemia, particularly since the A1C isalready widely familiar to clinicians as amarker of glycemic control. Moreover,the A1C has several advantages to theFPG, including greater convenience,since fasting is not required, evidence tosuggest greater preanalytical stability, andless day-to-day perturbations during pe-riods of stress and illness. These advan-tages, however, must be balanced bygreater cost, the limited availability ofA1C testing in certain regions of thedeveloping world, and the incompletecorrelation between A1C and average

glucose in certain individuals. In addi-tion, the A1C can be misleading in pa-tients with certain forms of anemia andhemoglobinopathies, which may alsohave unique ethnic or geographic distri-butions. For patients with a hemoglobin-opathy but normal red cell turnover, suchas sickle cell trait, an A1C assay withoutinterference from abnormal hemoglobinsshould be used (an updated list is avail-able at www.ngsp.org/prog/index3.html). For conditions with abnormal redcell turnover, such as anemias from he-molysis and iron deficiency, the diagnosisof diabetes must employ glucose criteriaexclusively.

The established glucose criteria forthe diagnosis of diabetes remain valid.These include the FPG and 2-h PG.Additionally, patients with severe hyper-glycemia such as those who present withsevere classic hyperglycemic symptomsor hyperglycemic crisis can continue to bediagnosed when a random (or casual)plasma glucose of $200 mg/dl (11.1mmol/l) is found. It is likely that in suchcases the health care professional wouldalso measure an A1C test as part of theinitial assessment of the severity of the di-abetes and that it would (in most cases) beabove the diagnostic cut point for diabe-tes. However, in rapidly evolving diabe-tes, such as the development of type 1diabetes in some children, A1C may notbe significantly elevated despite frankdiabetes.

Just as there is less than 100% con-cordance between the FPG and 2-h PGtests, there is not full concordance be-tween A1C and either glucose-basedtest. Analyses of NHANES data indicatethat, assuming universal screening of theundiagnosed, the A1C cut point of$6.5% identifies one-third fewer casesof undiagnosed diabetes than a fastingglucose cut point of $126 mg/dl (7.0mmol/l) (cdc website tbd). However, in

Table 3dCriteria for the diagnosis of diabetes

A1C$6.5%. The test should be performed in a laboratory using a method that is NGSP certifiedand standardized to the DCCT assay.*

ORFPG $126 mg/dl (7.0 mmol/l). Fasting is defined as no caloric intake for at least 8 h.*

OR2-h plasma glucose$200mg/dl (11.1mmol/l) during anOGTT. The test should be performed asdescribed by theWorld Health Organization, using a glucose load containing the equivalent of75 g anhydrous glucose dissolved in water.*

ORIn a patient with classic symptoms of hyperglycemia or hyperglycemic crisis, a random plasmaglucose $200 mg/dl (11.1 mmol/l).

*In the absence of unequivocal hyperglycemia, criteria 1–3 should be confirmed by repeat testing.


Position Statement

practice, a large portion of the populationwith type 2 diabetes remains unaware oftheir condition. Thus, it is conceivablethat the lower sensitivity of A1C at thedesignated cut point will be offset by thetest’s greater practicality, and that widerapplication of a more convenient test(A1C) may actually increase the numberof diagnoses made.

Further research is needed to bettercharacterize those patients whose glyce-mic status might be categorized differ-ently by two different tests (e.g., FPG andA1C), obtained in close temporal approx-imation. Such discordancemay arise frommeasurement variability, change overtime, or because A1C, FPG, and post-challenge glucose each measure differentphysiological processes. In the setting ofan elevated A1C but “nondiabetic” FPG,the likelihood of greater postprandial glu-cose levels or increased glycation ratesfor a given degree of hyperglycemia maybe present. In the opposite scenario (highFPG yet A1C below the diabetes cutpoint), augmented hepatic glucose pro-duction or reduced glycation rates maybe present.

As with most diagnostic tests, a testresult diagnostic of diabetes should berepeated to rule out laboratory error,unless the diagnosis is clear on clinicalgrounds, such as a patient with classicsymptoms of hyperglycemia or hypergly-cemic crisis. It is preferable that the sametest be repeated for confirmation, sincethere will be a greater likelihood of con-currence in this case. For example, if theA1C is 7.0% and a repeat result is 6.8%,the diagnosis of diabetes is confirmed.However, there are scenarios in which re-sults of two different tests (e.g., FPG andA1C) are available for the same patient. Inthis situation, if the two different tests areboth above the diagnostic thresholds, thediagnosis of diabetes is confirmed.

On the other hand, when two differ-ent tests are available in an individual andthe results are discordant, the test whoseresult 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 diabetescriterion of the A1C (two results $6.5%)but not the FPG (,126 mg/dl or 7.0mmol/l), or vice versa, that person shouldbe considered to have diabetes. Admit-tedly, in most circumstance the “nondia-betic” test is likely to be in a range veryclose to the threshold that defines diabetes.

Since there is preanalytic and analyticvariability of all the tests, it is also possible

that 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 decision about which test to useto assess a specific patient for diabetesshould be at the discretion of the healthcare professional, taking into account theavailability and practicality of testing anindividual patient or groups of patients.Perhaps more important than which di-agnostic test is used, is that the testing fordiabetes be performed when indicated.There is discouraging evidence indicatingthat many at-risk patients still do not re-ceive adequate testing and counseling forthis increasingly common disease, or for itsfrequently accompanying cardiovascularrisk factors. The current diagnostic criteriafor diabetes are summarized in Table 3.

Diagnosis of gestational diabetesGDM carries risks for the mother andneonate. The Hyperglycemia and AdversePregnancy Outcomes (HAPO) study(11), a large-scale (;25,000 pregnantwomen) multinational epidemiologicstudy, demonstrated that risk of adversematernal, fetal, and neonatal outcomescontinuously increased as a function ofmaternal glycemia at 24-28 weeks, evenwithin ranges previously considered nor-mal for pregnancy. For most complica-tions, there was no threshold for risk.These results have led to careful reconsid-eration of the diagnostic criteria for GDM.After deliberations in 2008-2009, theIADPSG, an international consensusgroup with representatives from multipleobstetrical and diabetes organizations, in-cluding ADA, developed revised recom-mendations for diagnosing GDM. Thegroup recommended that all women notknown to have diabetes undergo a 75-gOGTT at 24-28 weeks of gestation. Addi-tionally, the group developed diagnosticcutpoints for the fasting, 1-h, and 2-hplasma glucose measurements that con-veyed an odds ratio for adverse outcomesof at least 1.75 compared with womenwith mean glucose levels in the HAPOstudy. Current screening and diagnosticstrategies, based on the IADPSG state-ment (12), are outlined in Table 4.

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 ofoptimizing 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 cutpoints (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 diag-nostic criteria and that found modestbenefits (13,14). The frequency of theirfollow-up and blood glucose monitoringis not yet clear but likely to be less inten-sive than women diagnosed by the oldercriteria. Additional well-designed clinicalstudies are needed to determine the op-timal intensity of monitoring and treat-ment of women with GDM diagnosedby the new criteria (that would nothave met the prior definition of GDM).It is important to note that 80-90% ofwomen in both of the mild GDM studies(whose glucose values overlapped withthe thresholds recommended herein)could be managed with lifestyle therapyalone.

Table 4dScreening for and diagnosis ofGDM

Perform a 75-g OGTT, with plasma glucosemeasurement fasting and at 1 and 2 h, at24-28 of weeks gestation in women notpreviously diagnosed with overt diabetes.

The OGTT should be performed in themorning after an overnight fast of at least8 h.

The diagnosis of GDM ismade when any of thefollowing plasma glucose values areexceeded

c Fasting: $92 mg/dl (5.1 mmol/l)c 1 h: $180 mg/dl (10.0 mmol/l)c 2 h: $153 mg/dl (8.5 mmol/l)



References1. Expert Committee on the Diagnosis and

Classification of Diabetes Mellitus. Reportof the Expert Committee on the Diagnosisand Classification of Diabetes Mellitus.Diabetes Care 1997;20:1183–1197

2. Genuth S, Alberti KG, Bennett P, Buse J,Defronzo R, Kahn R, Kitzmiller J, KnowlerWC, Lebovitz H, Lernmark A, Nathan D,Palmer J, Rizza R, Saudek C, Shaw J,Steffes M, Stern M, Tuomilehto J, ZimmetP, Expert Committee on the Diagnosis andClassification of Diabetes Mellitus2, theExpert Committee on the Diagnosis andClassification of Diabetes Mellitus. Fol-low-up report on the diagnosis of diabetesmellitus. Diabetes Care 2003;26:3160–3167

3. International Expert Committee. Inter-national Expert Committee report on therole of the A1C assay in the diagnosis ofdiabetes. Diabetes Care 2009;32:1327–1334

4. Edelman D, Olsen MK, Dudley TK, HarrisAC, Oddone EZ. Utility of hemoglobinA1c in predicting diabetes risk. J Gen In-tern Med 2004;19:1175–1180

5. Pradhan AD, Rifai N, Buring JE, RidkerPM. Hemoglobin A1c predicts diabetesbut not cardiovascular disease in non-diabetic women. Am J Med 2007;120:720–727

6. Sato KK, Hayashi T, Harita N, Yoneda T,Nakamura Y, Endo G, Kambe H. Com-bined measurement of fasting plasmaglucose and A1C is effective for the pre-diction of type 2 diabetes: the KansaiHealthcare Study. Diabetes Care 2009;32:644–646

7. Shimazaki T, Kadowaki T, Ohyama Y,Ohe K, Kubota K. Hemoglobin A1c(HbA1c) predicts future drug treatmentfor diabetes mellitus: a follow-up studyusing routine clinical data in a Japaneseuniversity hospital. Translational Re-search 2007;149:196–204

8. Geiss LS, Pan L, Cadwell B, Gregg EW,Benjamin SM, Engelgau MM. Changes inincidence of diabetes in U.S. adults,1997–2003. Am J Prev Med 2006;30:371–377

9. Knowler WC, Barrett-Connor E, FowlerSE, Hamman RF, Lachin JM, Walker EA,Nathan DM, Diabetes Prevention ProgramResearch Group. Reduction in the in-cidence of type 2 diabetes with lifestyleintervention or metformin. N Engl J Med2002;346:393–403

10. Droumaguet C, Balkau B, Simon D, CacesE, Tichet J, Charles MA, Eschwege E, theDESIR Study Group. Use of HbA1c inpredicting progression to diabetes inFrench men and women: data from anEpidemiological Study on the Insulin

Resistance Syndrome (DESIR) DiabetesCare 2006;29:1619–1625.

11. Metzger BE, Lowe LP, Dyer AR, TrimbleER, Chaovarindr U, Coustan DR, HaddenDR, McCance DR, Hod M, McIntyre HD,Oats JJ, Persson B, Rogers MS, Sacks DA.Hyperglycemia and adverse pregnancyoutcomes. N Engl J Med 2008;358:1991–2002

12. Metzger BE, Gabbe SG, Persson B,Buchanan TA, Catalano PA, Damm P,Dyer AR, Leiva A, Hod M, Kitzmiler JL,Lowe LP, McIntyre HD, Oats JJ, Omori Y,Schmidt MI. International Association ofDiabetes and Pregnancy Study Groupsrecommendations on the diagnosis andclassification of hyperglycemia in preg-nancy. Diabetes Care 2010;33:676–682

13. Landon MB, Spong CY, Thom E,Carpenter MW, Ramin SM, Casey B,Wapner RJ, Varner MW, Rouse DJ, ThorpJM, Jr., Sciscione A, Catalano P, Harper M,Saade G, Lain KY, Sorokin Y, PeacemanAM, Tolosa JE, Anderson GB. A multi-center, randomized trial of treatment formild gestational diabetes. N Engl J Med2009;361:1339–1348

14. Crowther CA, Hiller JE, Moss JR, McPheeAJ, Jeffries WS, Robinson JS. Effect oftreatment of gestational diabetes mellituson pregnancy outcomes. N Engl J Med2005;352:2477–2486


Position Statement

DiabetesManagement at Camps forChildrenWith DiabetesAMERICAN DIABETES ASSOCIATION

S ince Leonard F.C. Wendt, MD,opened the doors of the first di-abetes camp in Michigan in 1925,

the concept of specialized residential andday camps for children with diabetes hasbecome widespread throughout the U.S.and many other parts of the world. In2011, approximately 30,000 children at-tended diabetes camps in North Americaand over 16,000 more campers partici-pated in one of the 180 diabetes campsthroughout the rest of the world.

The mission of camps specialized forchildren and youth with diabetes is tofacilitate a traditional camping experiencein a medically safe environment. Anequally important goal is to enable chil-dren with diabetes to meet and share theirexperiences with one another while theylearn to be more responsible for their con-dition. For this to occur, a skilled medicaland camping staff must be available toensure optimal safety and an integratedcamping/educational experience.

The recommendations for diabetesmanagement of children at a diabetescamp are not significantly different fromwhat has been outlined by the AmericanDiabetes Association (the Association) asthe standards of care for people with type1 diabetes (1) or for children with diabe-tes in the school or day care setting (2). Ingeneral, the diabetes camping experienceis short term and is most often associatedwith increased physical activity and morecontrolled access to food relative to thatexperienced at home. Thus, while away atcamp, glycemic control goals are more re-lated to avoiding blood glucose extremesthan optimizing overall glycemic control(3,4).Themanagementprotocol aims tobal-ance insulin dosage with activity level andfood intake so that blood glucose levelsstay within a safe target range, especially

with respect to the prevention and man-agement of hypoglycemia (5).

Each camper should have a standard-ized comprehensive health history formcompleted by his/her family and a healthevaluation form (6) completed by the di-abetes care provider that details the camp-er’s past medical history, immunizationrecord, and diabetes regimen. The homeinsulin regimen should be recorded foreach camper, including type(s) of insulinused, number and timing of insulin injec-tions (if on shots), and insulin pumpbasal, bolus, and correction dose settings(if on an insulin pump). Records for in-sulin dosages and blood glucose valuesfor the week immediately before campshould be provided as a baseline. Addi-tional medical information, such as priordiabetes-related illnesses and hospitaliza-tions, history of severe hypoglycemia,previous hemoglobin A1C levels, othermedications, significant medical con-ditions, and psychological issues alsoshould be available to camp personneland reviewed with diligence by those re-sponsible for the health and well-being ofthe individual camper.

During camp, a record of the camper’sdiabetes care progress should be docu-mented daily. All blood glucose valuesand insulin dosages should be recordedin a format that allows for review and anal-ysis to determine whether alterations inthe diabetes regimen are required duringthe camp stay. A record of the degree ofactivity and food intakemay also be helpfulin determining subsequent alterations inthe diabetes regimen. It is imperativethat the medical staff have advancedknowledge about the exercise scheduleand the meal plan at camp so that theycan make appropriate insulin dosage ad-justments. Inadvertent schedule delays or

schedule changes (such as for rainyweather) can have a significant impacton the risk of hypoglycemia as insulindosing at the previous meal takes into ac-count the planned activities. If a low-,moderate-, or high-level activity event isoriginally planned, a replacement activitywith an equivalent activity level shouldbe substituted when possible.

To ensure safety and optimal diabetesmanagement, blood glucose testing ma-terials and treatment supplies for hypo-glycemia should be readily available tocampers at all times. Multiple bloodglucose determinations should be madeand recorded throughout each 24-h pe-riod: before meals; at bedtime; before, af-ter, or during prolonged and strenuousactivity; in the middle of the night, whenindicated for prior hypoglycemia; after aninsulin pump site change; and after extradoses of insulin. Use of a continuousglucose monitoring system (CGMS) doesnot preclude the need to test finger-stickblood glucose.

Because exercise may still impactblood glucose 12–18 h after completion,campers who have repeated lows duringexercise may also need nocturnal testing.Campers with a bedtime blood glucoselevel,100 mg/dL and campers on an in-sulin pump with a blood glucose .240mg/dL should have their blood glucoserechecked overnight. The interventionfor campers with an overnight blood glu-cose level ,100 mg/dL should be deter-mined based on their insulin regimen andrisk for nocturnal hypoglycemia. Camp-ers on insulin pumpswith a blood glucose.240 mg/dL should follow an estab-lished pump protocol for ketone testingand changing of the insulin pump site.Campers should be encouraged to checkblood glucose levels at times other thanthe routine times if they have symptomsof hypo-/hyperglycemia or if they haveother physical complaints. These recom-mendations imply that there is adequatestaffing and that they have received trainingin blood glucose monitoring procedures aswell as the indications and treatment pro-tocols for hypo-/hyperglycemic events.

Every attempt should be made tofollow the home insulin regimen of eachcamper as closely as possible. If a camper’s


This updated position statement was peer reviewed by the Professional Practice Committee in September,2011, and approved by the Executive Committee of the American Diabetes Association inNovember, 2011.





blood glucose record prior to camp indi-cates tight glucose control and a low ac-tivity level, it may be advisable to decreasethe insulin dosage in anticipation of theincreased activity. Supervision of eachand every insulin administration is im-portant to ensure camper safety and com-pliance with the prescribed insulin dose.Hypoglycemia may occur at the begin-ning of camp because of increased phys-ical activity, failure to have free access tofood, or other conditions such as a majorchange in altitude. Other alterations in in-sulin dosage may need to be made for ex-treme physical activity, such as prolongedhikes or active water sports.

A rising percentage (and often a ma-jority) of children at camp manage theirdiabetes with an insulin pump, with al-most all of the remaining children on asubcutaneous basal/bolus insulin regimen.The camp medical director and otherappropriate camp staff should be familiarwith the programming of insulin pumps,the replacement of insulin pump infusionsets, and insulin adjustments using abasal/bolus insulin regimen or an insulinpump. The medical staff should ensurethat adequate backup pump supplies, in-cluding extra batteries, reservoirs, andcatheter sets, are available for the durationof camp.

If major alterations of a camper’s reg-imen appear to be indicated, such as add-ing an additional insulin injection(s) orchanging an insulin type, it is importantto discuss this with the camper and thefamily in addition to the child’s local di-abetes care provider before the change ismade. A record of the blood glucose val-ues, insulin doses, and other medical careprovided at camp, with an additionalcopy for the family to share with their pri-mary diabetes team (if they choose),should be available to (and discussedwith) the family at the end of camp. Forcampers returning home by bus or car-pool, the record should be sent with thecamper or mailed to his/her family. Pa-rents and campers should be advised toreturn to their precamp regimen oncethey are home, unless the alterations ap-pear to significantly improve glycemiccontrol. In this circumstance, the familyshould seek the guidance of its primarydiabetes team.

Dietary planning at camp should beoverseen by a registered dietitian. Mealsshould be given at set times each day andshould accommodate special dietaryneeds, when needed, especially those re-lated to food allergies and the increasing

incidence of celiac disease in the diabeticpopulation. Snacks between meals may beappropriate to prevent hypoglycemia, es-pecially in the youngest campers whomaynot recognize their hypoglycemic symp-toms. These meals and snacks should bebalanced, and their composition (specifi-cally the carbohydrate content) should bemade known to campers and staff. Car-bohydrate counting is optimally presentedin grams and should be as exact as possible(not rounded to the nearest completeserving or 15 g). The carbohydrate com-ponent of food should be taught to camp-ers, according to their developmentallevel, to enable them to learn how tobalance food and activity. Supervision ofthe food intake of children by counselorsensures that the campers are consumingadequate nutrition.

A formal relationship with a nearbymedical facility should be secured for eachcamp so that camp medical staff has theability to refer to this facility for prompttreatment of medical emergencies. (TheAmerican Camp Association requires thenotification of all emergency medical sup-port systems local to the camp.) If the campis located in a remote area, an arrangementshould be made with a medical helicopteror fixed-wing aircraft to provide rapidtransport if necessary.

Universal precautions including Oc-cupational Safety & Health Association(OSHA) regulations, Clinical LaboratoryImprovement Amendments (CLIA)standards, and state regulations must befollowed by all, with gloves worn for allprocedures that involve blood draws andappropriate containers placed throughoutthe camp to dispose of sharps withouthazard. Retractable single-use lancets andglucose meters in which blood does nottouch the machine itself are preferablefor group testing. No lancing device thatcan be reset and used again should beavailable to campers. Retractable insulinsyringe/pen needles may be considered tofurther reduce the risk of needle sticksamong campers and staff. Insulin pensare for single person use and should neverbe shared between two individuals. Careshould also be taken to ensure that insulinpumps are individually labeled so thatwhen they are disconnected (for swim-ming or bathing), the proper pump is re-connected to the proper camper to preventfluid contamination and improper insulinadministration. Whenever possible, bloodglucose meters should be assigned to anindividual person due to the risk of blood-borne pathogen contamination from blood

on the surface of the meter (7). If bloodglucose meters must be shared, the devicemust be cleaned and disinfected after everyuse, per the manufacturer instructions, toprevent potential cross contamination ofinfectious agents. Glucose meters shouldbe calibrated regularly using control solu-tion to verify accuracy (frequency shouldbe per the manufacturer instructions).

MEDICAL STAFFCOMPOSITION ANDSTAFF TRAININGdIt is imperativethat each camp have a medical directorwho is a physician with expertise in man-aging type 1 and type 2 diabetes. Themedical director or his/her on-site licenseddesignee ultimately is responsible for thedaily review of blood glucose results, in-sulin logs, and other prescribed medica-tions of all campers and staff with diabetesto make appropriate adjustments. Themedical director or the on-site licenseddesignee also is responsible for providingguidance in all medical emergencies andshould ensure that the medical program isintegrated into the overall camping expe-rience. One licensed physician must be onsite at all times for resident camp programsand available on call at all times for a daycamp program.

The medical staff can be comprisedof licensed healthcare professionals andnonhealthcare professionals with an in-terest in diabetes. Physicians, medicalresidents, midlevel providers (physicianassistants and advanced practice nurses),diabetes educators, pharmacists, andnurses should also be encouraged toparticipate. In addition, registered dieti-tians with expertise in diabetes shouldhave input into the design of the menuand the education program. It is beneficialto include some medical, nursing, phar-macy, physician assistant, nurse practi-tioner, and dietetic students as volunteercounselors or junior medical staff to learnabout diabetes as well as the needs ofchildren with a chronic disease.

All camp staff, including medical,nursing, nutrition, and other volunteer orpaid staff, should undergo backgroundchecks to ensure the appropriateness of theirworking with children. All staff should re-ceive training concerning routine diabetesmanagement, issues related to lifestylemodification for type 2 diabetes, and thetreatment of diabetes-related emergen-cies (hypoglycemia or ketosis) beforecamp begins. Camp policies and job de-scriptions for staff should be understoodand available in print before the start of


Position Statement

camp. All camp staff should be familiarwith the signs and symptoms of hypo-/hyperglycemia, indications for bloodglucose testing, and treatment of hypogly-cemia, including the administration ofglucagon to treat severe hypoglycemia(5,8). Competency testing of these skillsfor staff medically responsible for thecampers is strongly suggested. All diabetessupplies should be monitored and distrib-uted by responsible medical staff.

Reliable communication methods toallow contact with on-site medical staffshould exist in every activity area. Suppliesfor routine first aid and for the treatmentof intercurrent illnesses, such as allergies,asthma, sore throats, diarrhea/vomiting,and minor trauma, should be available.All medical treatment should be recordedin both the camper’s file and in the yearlycamp medical log.

TREATMENT OF DIABETES-RELATED EMERGENCIES

HypoglycemiaGlucagon or intravenous glucose solu-tions must be available for administrationby trained camp personnel for treatmentof severe hypoglycemia. All possiblemeasures should be taken to avert severehypoglycemia. These measures may in-clude nighttime blood glucose testing,decreasing insulin dosages for extremeactivity, and altering insulin regimens forcampers with prior severe hypoglycemia.Extra snacks should be provided to chil-dren with blood glucose levels,100 mg/dLat bedtime. Additional snacks or modifi-cations of insulin for children with bloodglucose levels ,80 mg/dL should also beconsidered.

A set protocol for the treatment ofmild-to-moderate hypoglycemia withoral glucose at other times should befollowed so that hypoglycemia is consis-tently managed. Repeat blood glucosetesting should be performed within 15–20 min to ensure resolution of hypogly-cemia.

KetosisIt may be possible to treat mild-to-moderate diabetic ketosis at camp. Urineor blood should be measured for thepresence of ketones if a camper has per-sistent hyperglycemia (blood glucoselevel .240 mg/dL [13.3 mmol/l]) or if acamper has an intercurrent illness, re-gardless of blood glucose level. Oral orintravenous hydration (if vomiting)should be administered, and adequate

insulin should be given to reverse ketosis.A flow sheet should be produced to doc-ument the progress of the treatment reg-imen. Referral to an appropriate medicalfacility is required if vomiting and ketosisdo not resolve promptly.

WRITTEN CAMPMANAGEMENT PLANdA writtenplan that includes camp policies andmedical management procedures mustbe available at camp. It should be writtenor reviewed by the camp medical directorin collaboration with others, such as thecamp program director, members of thecamp oversight and/or policy commit-tees, local pediatric endocrinologists anddiabetes educators, etc. The plan mustadhere to the American Diabetes Associ-ation’s standards of medical care and theAmerican Camp Association accredita-tion standards. All medical staff shouldreview this management plan beforecamp begins.

The written medical management planshould include information about:

c General diabetes managementc Insulin injections/pump therapyc Blood glucose monitoring and ketonetesting

c Nutrition, timing, and content of mealsand snacks

c Routine and special activitiesc Hypoglycemia and treatmentc Hyperglycemia/ketosis and treatmentc Medical formsc Assessment and treatment of intercur-rent illness

c Pharmacy compendiumc Universal precautions and policies forneedle sticks and handling of infectiouswaste

c Psychological issues at campc Quality control of medical equipmentaccording to OSHA and CLIA stand-ards

c Incident/accident reportingc When to notify parents/guardians, pri-mary care physician, and diabetes careprovider

c Policies for camp closure and returninghome

In addition, camp policies shouldcover emergency procedures (e.g., medi-cal and natural disasters), out-of-campexcursions, and the prevention of physi-cal, sexual, and psychological abuse. Arisk management plan should also bedeveloped and understood by all campstaff. The ADA’s Camp Implementation

Guide Modules (9) includes a variety ofresources including sample policies, jobdescriptions, and medical forms.

DIABETES EDUCATION ANDPSYCHOLOGICAL ISSUESdThecamp setting is an ideal place for teachingdiabetes self-management skills. Educa-tion programs should be developmentallyappropriate. Examples of educational top-ics suitable for the camp setting include:

c Blood glucose monitoringc Recognition and management of hypo-/hyperglycemia and ketosis

c Insulin types and administration tech-niques

c Carbohydrate countingc Insulin dosage adjustment based on nu-trition and activity schedules

c Insulin pump trouble shooting andproblem solving

c The importance of diabetes controlc Healthy lifestyles issues, including in-tegration of healthy eating, physical ac-tivity, and relaxation

c Problem-solving skills for caring fordiabetes at home versus camp

c Life skills for independent livingc Stress management and coping skillsc Sexual health and preconception issuesc Diabetes complicationsc New therapies including technologies

Medical personnel with the aid ofon-site psychologists/social workers, ifavailable, should aim to improve the psy-chological well-being of campers. Thesestaff members should be willing to addressspecific and general psychosocial issuesand be able to offer suggestions for sub-sequent follow-up if indicated. Individu-alized attentionmay be needed for camperswith type 2 versus type 1 diabetes.

RESEARCH AT CAMPdClinical re-search is often performed and encouragedat diabetes camps. However, if such proj-ects are to be done, they must not in-terfere with the integrity of the campingprogram. All research conducted in thecamp setting should be minimally inva-sive to the camping experience. All stud-ies should be approved by an institutionalreview board in good standing and by thecamp medical and program director be-fore the camping session. Parents andcampers must be provided the consentform, a summary/synopsis of the researchprotocol, and the ability to contact theprincipal investigator before consenting toenter the research study. Informed consent


American Diabetes Association

from parents or guardians and assent fromthe camper must be obtained, preferablybefore arrival at camp.

OTHERdAt times, industries related todiabetes may wish to have a presence atcamp. Camp medical staff and adminis-trative personnel should develop policiesfor visits from industries while camp is insession. Industry representatives seekingto have a presence at camp should besubject to the same background checksand standards outlined by the Association.Employees of industries should be en-couraged to participate at camp for theirexpertise, ability to educate others, andadded resources, while understandingthat their role is to support the experienceof the campers rather than to solicit orpromote their individual product.

CONCLUSIONSdCamps for chil-dren and youth focused on diabetes areinvaluable. Most camps have a high re-turn rate for campers, many of whom goon to become counselors, medical pro-fessionals, staff, and role models forcampers. Thus, it is reasonable to assumethat they have benefited not only from thecamp experience but also from the friend-ships that have developed from being in

an environmentwhere the norm is to havediabetes. Providing high-standard diabe-tes care is imperative to maximize theexperience offered by camps specializedfor children with diabetes. Using theactive camping environment as a teachingopportunity is an invaluable way forchildren with diabetes to gain skills inmanaging their disease within the sup-portive camp community.

AcknowledgmentsdThe original version ofthis Position Statement was prepared by Fran-cine Kaufman, MD, Desmond Schatz, MD, andJanet Silverstein, MD, and approved in 1998.The current revision was prepared by LowellSchmeltz, MD, with contribution from RussKolski, RN, Chair, and other members of theADA National Camp and Youth Subcommittee.

References1. American Diabetes Association: Standards

of medical care in diabetesd2012 (PositionStatement). Diabetes Care 2012;35(Suppl.1):S11–S63

2. American Diabetes Association. Diabetescare in the school and day care setting. Di-abetes Care 2012;35(Suppl. 1):S76–S80

3. The Diabetes Control and ComplicationsTrial Research Group. The effect of intensive

treatment of diabetes on the developmentand progression of long-term complica-tions in insulin-dependent diabetes melli-tus. N Engl J Med 1993;329:977–986

4. Diabetes Control and Complications TrialResearch Group. Effect of intensive diabetestreatment on the development and pro-gression of long-term complications in ado-lescents with insulin-dependent diabetesmellitus: Diabetes Control and Complica-tions Trial. J Pediatr 1994;125:177–188

5. Cryer PE, Davis SN, Shamoon H. Hypo-glycemia in diabetes. Diabetes Care 2003;26:1902–1912

6. American Academy of Pediatrics Commit-tee on School Health; American Academyof Pediatrics Section on School Health.Health appraisal guidelines for day campsand resident camps. Pediatrics 2005;115:1770–1773

7. Centers for Disease Control. Infection pre-vention during blood glucose monitor-ing and insulin administration [articleonline]. Available from http://www.cdc.gov/injectionsafety/blood-glucose-monitoring.html. Accessed 7 August 2011.

8. American Diabetes Association. MedicalManagement of Type 1 Diabetes. 4th ed.Alexandria, VA, American Diabetes Associ-ation, 2008

9. American Diabetes Association. Camp Im-plementation Guide Modules. Alexandria,VA, American Diabetes Association, 2005


Position Statement

Diabetes Care in the School andDayCareSettingAMERICAN DIABETES ASSOCIATION

D iabetes is one of the most commonchronic diseases of childhood (1).There are ;215,000 individu-

als ,20 years of age with diabetes inthe U.S. (2). The majority of these youngpeople attend school and/or some typeof day care and need knowledgeablestaff to provide a safe school environ-ment. Both parents and the health careteam should work together to provideschool systems and day care providerswith the information necessary to allowchildren with diabetes to participatefully and safely in the school experience(3,4).

DIABETES ANDTHE LAWdFederal laws that protectchildren with diabetes include Section504 of the Rehabilitation Act of 1973(5), the Individuals with Disabilities Edu-cation Act (originally the Education forAll Handicapped Children Act of 1975)(6), and the Americans with DisabilitiesAct (7). Under these laws, diabetes hasbeen considered to be a disability, and itis illegal for schools and/or day care cen-ters to discriminate against children withdisabilities. In addition, any school thatreceives federal funding or any facilityconsidered open to the public must rea-sonably accommodate the special needsof children with diabetes. Indeed, federallaw requires an individualized assessmentof any child with diabetes. The requiredaccommodations should be documentedin a written plan developed under the ap-plicable federal law such as a Section 504Plan or Individualized Education Pro-gram (IEP). The needs of a student withdiabetes should be provided for withinthe child’s usual school setting with aslittle disruption to the school’s and thechild’s routine as possible and allowing

the child full participation in all schoolactivities (8,9).

Despite these protections, children inthe school and day care setting still facediscrimination. For example, some daycare centers may refuse admission tochildren with diabetes, and children inthe classroom may not be provided theassistance necessary to monitor bloodglucose and administer insulin and maybe prohibited from eating needed snacks.The American Diabetes Association worksto ensure the safe and fair treatment ofchildren with diabetes in the school andday care setting (10–15) (www.diabetes.org/schooldiscrimination).

Diabetes care in schoolsAppropriate diabetes care in the schooland day care setting is necessary for thechild’s immediate safety, long-term wellbeing, and optimal academic perfor-mance. The Diabetes Control and Com-plications Trial showed a significant linkbetween blood glucose control and laterdevelopment of diabetes complications,with improved glycemic control decreas-ing the risk of these complications(16,17). To achieve glycemic control, achild must check blood glucose fre-quently, monitor food intake, take medi-cations, and engage in regular physicalactivity. Insulin is usually taken in multi-ple daily injections or through an infusionpump. Crucial to achieving glycemic con-trol is an understanding of the effects ofphysical activity, nutrition therapy, andinsulin on blood glucose levels.

To facilitate the appropriate care ofthe student with diabetes, the schoolnurse as well as other school and day carepersonnel must have an understanding ofdiabetes and must be trained in its man-agement and in the treatment of diabetes

emergencies (3,18,19,20,34,36). Knowl-edgeable trained personnel are essentialif the student is to avoid the immediatehealth risks of low blood glucose and toachieve the metabolic control required todecrease risks for later development of di-abetes complications (3,20). Studies haveshown that the majority of school person-nel have an inadequate understanding ofdiabetes (21,22). Consequently, diabeteseducation must be targeted toward daycare providers, teachers, and other schoolpersonnel who interact with the child, in-cluding school administrators, schoolnurses, coaches, health aides, bus drivers,secretaries, etc. (3,20). Current recom-mendations and up-to-date resources re-garding appropriate care for children withdiabetes in the school are universally avail-able to all school personnel (3,23).

The purpose of this position statementis to provide recommendations for themanagement of children with diabetes inthe school and day care setting.

GENERAL GUIDELINES FORTHE CARE OF THE CHILD INTHE SCHOOL AND DAY CARESETTING

I. Diabetes medical managementplanAn individualized Diabetes Medical Man-agement Plan (DMMP) should be devel-oped by the student’s personal diabeteshealth care team with input from theparent/guardian. Inherent in this processare delineated responsibilities assumed byall parties, including the parent/guardian,the school personnel, and the student(3,24,25). These responsibilities are out-lined in this position statement. In addi-tion, the DMMP should be used as thebasis for the development of written edu-cation plans such as the Section 504 Planor the IEP. The DMMP should address thespecific needs of the child and providespecific instructions for each of the fol-lowing:


Originally approved 1998. Revised 2008.DOI: 10.2337/dc12-s076© 2012 by the American Diabetes Association. Readers may use this article as long as the work is properly




1. Blood glucose monitoring, includingthe frequency and circumstances re-quiring blood glucose checks, and useof continuous glucose monitoring ifutilized.

2. Insulin administration (if necessary),including doses/injection times pre-scribed for specific blood glucose val-ues and for carbohydrate intake, thestorage of insulin, and, when appro-priate, physician authorization of par-ent/guardian adjustments to insulindosage.

3. Meals and snacks, including food con-tent, amounts, and timing.

4. Symptoms and treatment of hypogly-cemia (low blood glucose), includingthe administration of glucagon if rec-ommended by the student’s treatingphysician.

5. Symptoms and treatment of hypergly-cemia (high blood glucose).

6. Checking for ketones and appropriateactions to take for abnormal ketonelevels, if requested by the student’shealth care provider.

7. Participation in physical activity.8. Emergency evacuation/school lock-

down instructions.

A sample DMMP (http://www.dia-betes.org/uedocuments/DMMP-finalformatted.pdf) may be accessed online andcustomized for each individual student.For detailed information on the symptomsand treatment of hypoglycemia and hy-perglycemia, refer to Medical Managementof Type 1 Diabetes (26). A brief descriptionof diabetes targeted to school and day carepersonnel is included in the APPENDIX; itmay be helpful to include this informationas an introduction to the DMMP.

II. Responsibilities of the variouscare providers (3)

A. The parent/guardian should providethe school or day care provider withthe following:

1. All materials, equipment, insulin,and other medication necessary fordiabetes care tasks, including bloodglucose monitoring, insulin admin-istration (if needed), and urine orblood ketone monitoring. The par-ent/guardian is responsible for themaintenance of the blood glucosemonitoring equipment (i.e., cleaningand performing controlled testingper the manufacturer’s instructions)and must provide materials necessary

to ensure proper disposal of materials.A separate logbook should be kept atschool with the diabetes supplies forthe staff or student to record bloodglucose and ketone results; blood glu-cose values should be transmitted tothe parent/guardian for review as oftenas requested. Some studentsmaintain arecord of blood glucose results in me-ter memory rather than recording in alogbook, especially if the same meter isused at home and at school.

2. The DMMP completed and signed bythe student’s personal diabetes healthcare team.

3. Supplies to treat hypoglycemia, in-cluding a source of glucose and a glu-cagon emergency kit, if indicated inthe DMMP.

4. Information about diabetes and theperformance of diabetes-relatedtasks.

5. Emergency phone numbers for theparent/guardian and the diabeteshealth care team so that the schoolcan contact these individuals withdiabetes-related questions and/or dur-ing emergencies.

6. Information about the student’s meal/snack schedule. The parent shouldwork with the school during theteacher preparation period before thebeginning of the school year or beforethe student returns to school after di-agnosis to coordinate this schedulewith that of the other students as closelyas possible. For young children, in-structions should be given for whenfood is provided during school partiesand other activities.

7. In most locations, and increasingly, asigned release of confidentiality fromthe legal guardian will be required sothat the health care team can com-municate with the school. Copiesshould be retained both at the schooland in the health care professionals’offices.

B. The school or day care providershould provide the following:

1. Opportunities for the appropriatelevel of ongoing training and diabeteseducation for the school nurse.

2. Training for school personnel as fol-lows: level 1 training for all schoolstaff members, which includes a basicoverview of diabetes, typical needsof a student with diabetes, recogni-tion of hypoglycemia and hyper-glycemia, and who to contact for

help; level 2 training for school staffmembers who have responsibilityfor a student or students with di-abetes, which includes all contentfrom level 1 plus recognition andtreatment of hypoglycemia and hy-perglycemia and required accom-modations for those students; andlevel 3 training for a small group ofschool staff members who will per-form student-specific routine andemergency care tasks such as bloodglucose monitoring, insulin adminis-tration, and glucagon administrationwhen a school nurse is not availableto perform these tasks andwhichwillinclude level 1 and 2 training as well.

3. Immediate accessibility to the treat-ment of hypoglycemia by a knowl-edgeable adult. The student shouldremain supervised until appropriatetreatment has been administered,and the treatment should be availableas close to where the student is aspossible.

4. Accessibility to scheduled insulin attimes set out in the student’s DMMPas well as immediate accessibility totreatment for hyperglycemia includinginsulin administration as set out by thestudent’s DMMP.

5. A location in the school that providesprivacy during blood glucose moni-toring and insulin administration, ifdesired by the student and family, orpermission for the student to checkhis or her blood glucose level andtake appropriate action to treat hy-poglycemia in the classroom or any-where the student is in conjunctionwith a school activity, if indicated inthe student’s DMMP.

6. School nurse and back-up trainedschool personnel who can checkblood glucose and ketones and ad-minister insulin, glucagon, and othermedications as indicated by the stu-dent’s DMMP.

7. School nurse and back-up trainedschool personnel responsible for thestudent who will know the scheduleof the student’s meals and snacks andwork with the parent/guardian tocoordinate this schedule with that ofthe other students as closely as pos-sible. This individual will also notifythe parent/guardian in advance ofany expected changes in the schoolschedule that affect the student’smeal times or exercise routine andwill remind young children of snacktimes.


Position Statement

8. Permission for self-sufficient and ca-pable students to carry equipment,supplies, medication, and snacks; toperform diabetes management tasks;and to have cell phone access to reachparent/guardian and health careprovider.

9. Permission for the student to see theschool nurse and other trainedschool personnel upon request.

10. Permission for the student to eat asnack anywhere, including the class-room or the school bus, if necessary toprevent or treat hypoglycemia.

11. Permission to miss school withoutconsequences for illness and requiredmedical appointments to monitor thestudent’s diabetes management. Thisshould be an excused absence with adoctor’s note, if required by usualschool policy.

12. Permission for the student to use therestroom and have access to fluids(i.e., water) as necessary.

13. An appropriate location for insulinand/or glucagon storage, if neces-sary.

14. A plan for the disposal of sharpsbased upon an agreement with thestudent’s family, local ordinances,and Universal Precaution Standards.

15. Information on serving size and ca-loric, carbohydrate, and fat contentof foods served in the school (27).

The school nurse should be the key co-ordinator and provider of care and shouldcoordinate the training of an adequatenumber of school personnel as specifiedabove and ensure that if the school nurse isnot present at least one adult is presentwho is trained to perform these proce-dures in a timely manner while thestudent is at school, on field trips, par-ticipating in school-sponsored extracur-ricular activities, and on transportationprovided by the school or day carefacility. This is needed in order to enablefull participation in school activities(3,18,20). These school personnelneed not be health care professionals(3,9,20,28,33,35).

It is the school’s responsibility to pro-vide appropriate training of an adequate

number of school staff on diabetes-relatedtasks and in the treatment of diabetesemergencies. This training should be pro-vided by the school nurse or anotherqualified health care professional with ex-pertise in diabetes. Members of the stu-dent’s diabetes health care team shouldprovide school personnel and parents/guardians with educational materialsfrom the American Diabetes Associationand other sources targeted to school per-sonnel and/or parents. Table 1 includes alisting of appropriate resources.

III. Expectations of the student indiabetes careChildren and youth should be allowed toprovide their own diabetes care at schoolto the extent that is appropriate based onthe student’s development and his or herexperience with diabetes. The extent ofthe student’s ability to participate in di-abetes care should be agreed upon by theschool personnel, the parent/guardian,and the health care team, as necessary.The ages at which children are able toperform self-care tasks are variable anddepend on the individual, and a child’scapabilities and willingness to provideself-care should be respected (18).

1. Toddlers and preschool-aged children:unable to perform diabetes tasks in-dependently and will need an adult toprovide all aspects of diabetes care.Many of these younger children willhave difficulty in recognizing hypo-glycemia, so it is important that schoolpersonnel are able to recognize andprovide prompt treatment. However,children in this age range can usuallydetermine which finger to prick, canchoose an injection site, and are gen-erally cooperative.

2. Elementary school–aged children: de-pending on the length of diagnosisand level of maturity, may be able toperform their own blood glucosechecks, but usually will require su-pervision. Older elementary school–aged children are generally beginningto self-administer insulin with super-vision and understand the effect ofinsulin, physical activity, and nutritionon blood glucose levels. Unless thechild has hypoglycemic unawareness,he or she should usually be able to letan adult know when experiencing hy-poglycemia.

3. Middle school and high school–agedchildren: usually able to provide self-care depending on the length of

Table 1dResources for teachers, child care providers, parents, and health professionals

Helping the Student with Diabetes Succeed: A Guide for School Personnel. National DiabetesEducation Program, 2003. Available at http://www.ndep.nih.gov/Diabetes/pubs/Youth_SchoolGuide.pdf

Diabetes Care Tasks at School: What Key Personnel Need to Know. Alexandria, VA, AmericanDiabetes Association, 2008. Available online at http://shopdiabetes.org/58-diabetes-care-tasks-at-school-what-key-personnel-need-to-know-2010-edition.aspx.

Your School & Your Rights: Protecting Children with Diabetes Against Discrimination in Schools andDay Care Centers. Alexandria, VA, American Diabetes Association, 2005 (brochure). Availableonline at http://www.diabetes.org/assets/pdfs/schools/your-school-your-right-2010.pdf.*

Children with Diabetes: Information for School and Child Care Providers. Alexandria, VA, AmericanDiabetes Association, 2004 (brochure). Available at http://shopdiabetes.org/42-children-with-diabetes-information-for-school-and-child-care-providers.aspx.*

ADA’s Safe at School campaign and information on how to keep children with diabetes safe atschool. Call 1-800-DIABETES and go to www.diabetes.org/living-with-diabetes/parents-and-kids/diabetes-care-at-school/safe-at-school

American Diabetes Association: Complete Guide to Diabetes. Alexandria, VA, American DiabetesAssociation, 2005. Available at http://shopdiabetes.org/114-american-diabetes-association-complete-guide.aspx.

Raising a Child with Diabetes: A Guide for Parents. Alexandria, VA, American Diabetes Association,2000. Available at http://shopdiabetes.org/137-ada-guide-to-raising-a-child-with-diabetes-2nd-edition.aspx.

Clarke W: Advocating for the child with diabetes. Diabetes Spectrum 12:230–236, 1999.School Discrimination Resources. Alexandria, VA, American Diabetes Association, 2006. Availableat http://www.diabetes.org/living-with-diabetes/know-your-rights/discrimination/school-discrimination/*

Every Day Wisdom: A Kit for Kids with Diabetes (and their parents). Alexandria, VA, AmericanDiabetes Association, 2000. Available at http://www.diabetes.org/living-with-diabetes/parents-and-kids/everyday-wisdom-kit.html

ADA’s Planet D, on-line information for children and youth with diabetes. Accessible at http://www.diabetes.org/living-with-diabetes/parents-and-kids/planet-d/

*Available in the American Diabetes Association’s Education Discrimination Packet by calling 1-800-DIABETES.



diagnosis and level of maturity butwill always need help when experi-encing severe hypoglycemia. Inde-pendence in older children should beencouraged to enable the child tomake his or her decisions about his orher own care.

Students’ competence and capabilityfor performing diabetes-related tasks areset out in the DMMP and then adapted tothe school setting by the school healthteam and the parent/guardian. At all ages,individuals with diabetes may requirehelp to perform a blood glucose checkwhen the blood glucose is low. In addi-tion, many individuals require a reminderto eat or drink during hypoglycemia andshould not be left unsupervised until suchtreatment has taken place and the bloodglucose value has returned to the normalrange. Ultimately, each person with di-abetes becomes responsible for all aspectsof routine care, and it is important forschool personnel to facilitate a student inreaching this goal. However, regardlessof a student’s ability to provide self-care,help will always be needed in the eventof a diabetes emergency.

MONITORING BLOODGLUCOSE IN THECLASSROOMdIt is best for a stu-dent with diabetes to monitor blood glu-cose levels and respond to the results asquickly and conveniently as possible.This is important to avoid medical prob-lems being worsened by a delay inmonitoring and treatment and to mini-mize educational problems caused bymissing instruction in the classroom.Accordingly, as stated earlier, a studentshould be permitted to monitor his orher blood glucose level and take appro-priate action to treat hypoglycemia andhyperglycemia in the classroom or any-where the student is in conjunctionwith a school activity, if preferred bythe student and indicated in the stu-dent’s DMMP (3,24). However, somestudents desire privacy for blood glu-cose monitoring and other diabetescare tasks, and this preference shouldalso be accommodated.

In summary, with proper planningand the education and training of schoolpersonnel, children and youth with di-abetes can fully participate in the schoolexperience. To this end, the family, thehealth care team, and the school shouldwork together to ensure a safe learningenvironment.

APPENDIX

Background information ondiabetes for school personnel (3)Diabetes is a serious, chronic disease thatimpairs the body’s ability to use food.Insulin, a hormone produced by thepancreas, helps the body convert foodinto energy. In people with diabetes, ei-ther the pancreas does not make insulinor the body cannot use insulin properly.Without insulin, the body’s main energysourcedglucosedcannot be used as fuel.Rather, glucose builds up in the blood.Over many years, high blood glucoselevels can cause damage to the eyes, kid-neys, nerves, heart, and blood vessels.

The majority of school-aged youthwith diabetes have type 1 diabetes. Peoplewith type 1 diabetes do not produce in-sulin and must receive insulin througheither injections or an insulin pump. In-sulin taken in this manner does not curediabetes and may cause the student’sblood glucose level to become danger-ously low. Type 2 diabetes, the mostcommon form of the disease, typicallyafflicting obese adults, has been shown tobe increasing in youth. This may be dueto the increase in obesity and decrease inphysical activity in young people. Stu-dents with type 2 diabetes may be able tocontrol their disease through diet andexercise alone or may require oral medi-cations and/or insulin injections. Allpeople with type 1 and type 2 diabetesmust carefully balance food, medica-tions, and activity level to keep bloodglucose levels as close to normal as pos-sible.

Low blood glucose (hypoglycemia) isthe most common immediate healthproblem for students with diabetes. Itoccurs when the body gets too much in-sulin, too little food, a delayed meal, ormore than the usual amount of exercise.Symptoms of mild to moderate hypogly-cemia include tremors, sweating, light-headedness, irritability, confusion, anddrowsiness. In younger children othersymptoms may include inattention, fallingasleep at inappropriate times, unexplainedbehavior, and temper tantrums. A studentwith this degree of hypoglycemia willneed to ingest carbohydrates promptlyand may require assistance. Severe hypo-glycemia, which is rare, may lead to un-consciousness and convulsions and can belife-threatening if not treated promptlywith glucagon as per the student’s DMMP(18,24,29,30,31).

High blood glucose (hyperglycemia)occurs when the body gets too little insulin,too much food, or too little exercise; it mayalso be caused by stress or an illness suchas a cold. The most common symptomsof hyperglycemia are thirst, frequent uri-nation, and blurry vision. If untreatedover a period of days, hyperglycemia andinsufficient insulin can lead to a seriouscondition called diabetic ketoacidosis(DKA), which is characterized by nausea,vomiting, and a high level of ketones in theblood and urine. For students using insulininfusion pumps, lack of insulin supplymaylead to DKAmore rapidly. DKA can be life-threatening and thus requires immediatemedical attention (32).

AcknowledgmentsdThe American DiabetesAssociation thanks the members of the healthcare professional volunteer writing group forthis updated statement: William Clarke, MD;Larry C. Deeb, MD; Paula Jameson, MSN,ARNP, CDE; Francine Kaufman, MD; Geor-geanna Klingensmith, MD; Desmond Schatz,MD; Janet H. Silverstein, MD; and Linda M.Siminerio, RN, PhD, CDE.

References1. American Diabetes Association: American

Diabetes Association Complete Guide to Di-abetes. 4th ed. Alexandria, VA, AmericanDiabetes Association, 2008

2. Centers for Disease Control and Pre-vention: National Diabetes Fact Sheet: Na-tional Estimates and General Informationon Diabetes and Prediabetes in the UnitedStates, 2011. Atlanta, GA, U.S. Depart-ment of Health and Human Services,Centers for Disease Control and Preven-tion, 2011

3. National Diabetes Education Program:Helping the Student with Diabetes Succeed: AGuide for School Personnel. Bethesda, MD,National Institutes of Health (NIH publi-cation no. 03-5127), 2003

4. Nabors L, Troillett A, Nash T, Masiulis B:School nurse perceptions of barriers andsupports for children with diabetes. J SchHealth 75: 119–124, 2005

5. 504 of the Rehabilitation Act of 1973, 29U.S.C. 794, implementing regulations at35 CFR Part 104

6. Individuals with Disabilities EducationAct, 20 U.S.C. 1400 et seq., implementingregulations at 34 CRF Part 300

7. Title II of the Americans with DisabilitiesAct of 1990, 42 U.S.C. 12134 et seq., im-plementing regulations at 28 CFR Part 35

8. Rapp J: Students with diabetes in schools.In Inquiry & Analysis. Alexandria, VA,National School Boards Association Councilof School Attorneys, June 2005


Position Statement

9. Arent S, Kaufman F: Federal laws anddiabetes management at school. SchoolNurse News, November 2004

10. Jesi Stuthard and ADA v. KindercareLearning Centers, Inc. Case no. C2-96-0185 (USCD South Ohio 8/96)

11. Calvin Davis and ADA v. LaPetite Academy,Inc. Case no. CIV97-0083-PHX-SMM(USCD Arizona 1997)

12. Agreement, Loudoun County PublicSchools (VA) and the Office for CivilRights, United States Department of Ed-ucation (Complaint nos. 11-99-1003, 11-99-1064, 11-99-1069, 1999)

13. Henderson County (NC) Pub. Schls., Com-plaint no. 11-00-1008, 34 IDLER 43(OCR 2000)

14. Rapp J, Arent S, Dimmick B, Jackson C:Legal Rights of Students with Diabetes. 2nded. Alexandria, VA, American DiabetesAssociation,October 2005, updatedOctober2009. Available from http://www.diabetes.org/living-with-diabetes/know-your-rights/for-lawyers/education-materials-for-lawyers/legal-rights-of-students-with-diabetes.html

15. Greene MA: Diabetes legal advocacycomes of age. Diabetes Spectr 19: 171–179, 2006

16. Diabetes Control and Complications TrialResearch Group: Effect of intensive di-abetes treatment on the development andprogression of long-term complications ininsulin-dependent diabetes mellitus. NEngl J Med 329: 977–986, 1993

17. Diabetes Control and Complications TrailResearch Group: Effect of intensive di-abetes treatment on the development andprogression of long-term complications inadolescentswith insulin-dependent diabetesmellitus. J Pediatr 125: 177–188, 1994

18. American Diabetes Association: Care ofchildren and adolescents with type 1 di-abetes (Position Statement). Diabetes Care28: 186–212, 2005

19. Barrett JC, Goodwin DK, Kendrick O:Nursing, food service, and the child withdiabetes. J Sch Nurs 18: 150–156, 2002

20. Jameson P: Developing diabetes trainingprograms for school personnel. SchoolNurse News, September 2004

21. Wysocki T, Meinhold P, Cox DJ, ClarkeWL: Survey of diabetes professionalsregarding developmental charges in di-abetes self-care. Diabetes Care 13: 65–68,1990

22. Lindsey R, Jarrett L, Hillman K: Elemen-tary schoolteachers’ understanding of di-abetes. Diabetes Educ 13: 312–314, 1987

23. American Diabetes Association: DiabetesCare Tasks at School: What Key PersonnelNeed to Know. Alexandria, VA, AmericanDiabetes Association, 2008 (available on-line at www.diabetes/schooltraining)

24. Jameson P: Helping students with di-abetes thrive in school. In On the Cut-ting Edge, American Dietetic Association’sDiabetes Care and Education PracticeGroup Newsletter. Summer 2006, p. 26–29

25. Owen S: Pediatric pumpsdbarriers andbreakthroughs. Pediatric Pumps 32 (Suppl.1), January/February 2006

26. American Diabetes Association: MedicalManagement of Type 1 Diabetes. 5th ed.Alexandria, VA, American Diabetes Asso-ciation, 2008

27. Accommodating Children with Special Di-etary Needs in the School Nutrition Program:Guidance for School Food Service Staff.Washington, DC, U.S. Department ofAgriculture Food and Nutrition Service,2001

28. American Diabetes Association: Safe atSchool Campaign Statement of Principlesendorsed by American Academy of Pedi-atrics, American Association of ClinicalEndocrinologists, American Associationof Diabetes Educators, American Dia-betes Association, American Dietetic

Association, Children with Diabetes, Dis-ability Rights Education Defense Fund,Juvenile Diabetes Research Foundation,Lawson Wilkins Pediatric Endocrine So-ciety, Pediatric EndocrineNursing Society,Endocrine Society [article online]. Avail-able from http://www.diabetes.org/advo-cacy-and-legalresources/discrimina-tion/safeatschoolprinciples.jsp

29. Evert A: Managing hypoglycemia in theschool setting. School Nurse News, No-vember 2005

30. Bulsara MD, Holman CD, David EA, JonesTW: The impact of a decade of changingtreatment on rates of severe hypoglycemiain a population-based cohort of childrenwith type 1 diabetes. Diabetes Care 27:2293–2298, 2004

31. Nabors L, Lehmkuhl H, Christos N,Andreone TF: Children with diabetes: per-ceptions of supports for self-managementat school. J Sch Health 73: 216–221,2003

32. Kaufman FR: Diabetes mellitus. PediatrRev 18: 383–392, 1997

33. Pediatric Endocrine Nursing Society:Children With Diabetes at School. Septem-ber 2005. Available from the PediatricEndocrinology Nursing Society, 7794Grow Dr., Pensacola, FL 32514

34. Committee on School Health, AmericanAcademy of Pediatrics Policy Statement:Guidance for the administration of medi-cation in school. Pediatrics 124: 1244–1251, 2009

35. Hellems MA, Clarke WL: Safe at school:a Virginia experience. Diabetes Care 30:1396–1398, 2007

36. American Medical Association: Report 4of the Council on Science and PublicHealth (A-08): Ensuring the Best In-SchoolCare for Children with Diabetes [articleonline], June 2008. Available at http://www.ama-assn.org/ama/pub/category/18643.html.



Diabetes and DrivingAMERICAN DIABETES ASSOCIATION

O f the nearly 19 million people in theU.S. with diagnosed diabetes (1), alarge percentage will seek or cur-

rently hold a license to drive. For many, adriver’s license is essential to work; takingcare of family; securing access to public andprivate facilities, services, and institutions;interacting with friends; attending classes;and/or performingmany other functions ofdaily life. Indeed, in many communitiesand areas of the U.S. the use of an automo-bile is the only (or the only feasible or af-fordable)means of transportation available.

There has been considerable debatewhether, and the extent to which, diabetesmay be a relevant factor in determiningdriver ability and eligibility for a license.This position statement addresses suchissues in light of current scientific andmedical evidence.

Sometimes people with a strong in-terest in road safety, including motor vehi-cle administrators, pedestrians, drivers,other road users, and employers, associateall diabetes with unsafe driving when infact most people with diabetes safely oper-ate motor vehicles without creating anymeaningful risk of injury to themselvesor others. When legitimate questions ariseabout the medical fitness of a person withdiabetes to drive, an individual assessment ofthat person’s diabetes managementdwithparticular emphasis on demonstrated abil-ity to detect and appropriately treat poten-tial hypoglycemiadis necessary in orderto determine any appropriate restrictions.The diagnosis of diabetes is not sufficientto make any judgments about individualdriver capacity.

This document provides an overviewof existing licensing rules for people withdiabetes, addresses the factors that impactdriving for this population, and identifiesgeneral guidelines for assessing driver fit-ness and determining appropriate licensingrestrictions.

LICENSINGREQUIREMENTSdPeople with dia-betes are currently subject to a great varietyof licensing requirements and restrictions.These licensing decisions occur at severalpoints and involve different levels andtypes of review, depending on the type ofdriving. Some states and local jurisdictionsimpose no special requirements for peoplewith diabetes. Other jurisdictions ask driv-ers with diabetes various questions abouttheir condition, including their manage-ment regimen and whether they have ex-perienced any diabetes-related problemsthat could affect their ability to safely oper-ate a motor vehicle. In some instances,answers to these questions result in restric-tions being placed on a person’s license, in-cluding restrictions on the type of vehicletheymay operate and/or where theymay op-erate that vehicle. In addition, the rules foroperating a commercial motor vehicle, andfor obtaining related license endorsements(such as rules restrictingoperationof a schoolbus or transport of passengers or hazardousmaterials) are quite different and in manyways more cumbersome for people with di-abetes, especially those who use insulin.

With the exception of commercialdriving in interstate commerce (Interstatecommercial driving is defined as trade,traffic or transportation in theUnited Statesbetween a place in a state and a placeoutside of such a state, between two placesin a state through another state or a placeoutside of the United States, or betweentwo places in a state as part of trade, trafficor transportation originating or terminat-ing outside the state or the United States[2]), which is subject to uniform federalregulation, both private and commercialdriving are subject to rules determined byindividual states. These rules vary widely,with each state taking its own approach todetermining medical fitness to drive andthe issuance of licenses. How diabetes is

identified,which people aremedically eval-uated, and what restrictions are placed onpeople who have experienced hypoglyce-mia or other problems related to diabetesall vary from state to state.

States identify drivers with diabetesin a number of ways. In at least 23 states,drivers are either asked directly if theyhave diabetes or are otherwise required toself-identify if they have diabetes. In otherstates drivers are asked some variation of aquestion about whether they have a con-dition that is likely to cause altered percep-tion or loss of consciousness while driving.In most states, when the answer to eitherquestion is yes, the driver is required tosubmit to a medical evaluation before heor she will be issued a license.

Medical evaluationDrivers whose medical conditions can leadto significantly impaired consciousness areevaluated for their fitness to continue todrive. For people with diabetes, this typi-cally occurswhen a person has experiencedhypoglycemia (3) behind the wheel, even ifthis did not result in a motor vehicle acci-dent. In some states this occurs as a resultof a policy to evaluate all people with di-abetes, even if there has been no triggeringevent. It can also occur when a person ex-periences severe hypoglycemia while notdriving and a physician reports the episodeto the licensing authority. In a handful ofstates, such reporting by physicians isman-datory. In most other states physicians arepermitted to make reports but are givendiscretion to determine when such reportsare necessary. Some states specify thatphysiciansmay voluntarily report those pa-tients who pose an imminent threat to pub-lic safety because they are driving againstmedical advice. Physicians and others re-quired to make reports to the licensing au-thority are usually providedwith immunityfrom civil and criminal actions resultingfrom the report.

When licensing authorities learnthat a driver has experienced an episodeof hypoglycemia that potentially affectedthe ability to drive, that driver is referredfor a medical evaluation and in manycases will lose driving privileges for a periodof time until cleared by the licensing au-thority. This period can range from 3 to 6months or longer. Some state laws allow forwaivers of the rules when the episode is aone-time event not likely to recur, for


Peer reviewed by the Professional Practice Committee, September 2011, and approved by the ExecutiveCommittee of the American Diabetes Association, November 2011.





example because of a change in medicationor episodes that occur only during sleep.

Medical evaluation procedures varyand range from a simple confirmation ofthe person’s diabetes from a physician to amore elaborate process involving a statemedical advisory board, hearings, andpresentation and assessment of medicalevidence. Some states convene medicaladvisory boards with nurses and physi-cians of different specialties who reviewand make recommendations concerningthe licensing of people with diabetes andother medical conditions. In other states,licensing decisions are made by adminis-trative staff with little or no medical train-ing and with little or no review by amedical review board or by a physicianor physicians with any relevant expertiseconcerning medical conditions presentedby individual applicants.

The medical evaluation process forcommercial drivers occurs at predeter-mined intervals, typically every 2 years.Unlike noncommercial licenses, theseregular evaluations are not linked toepisodes of severe hypoglycemia but arepart of an ongoing fitness evaluation forjobs requiring commercial driving. The fed-eral government has no diabetes-specificrestrictions for individuals who managetheir disease with diet, exercise, and/ororal medication. It offers an exemptionprogram for insulin-using interstate com-mercial drivers and issues medical certifi-cates to qualified drivers. Factors in thefederal commercial driving medical evalu-ation include a review of diabetes history,medications, hospitalizations, blood glu-cose history, and tests for various com-plications and an assessment of driverunderstanding of diabetes and willingnessto monitor their condition.

SCIENCE OF DIABETES ANDDRIVINGdHypoglycemia indicatingan impaired ability to drive, retinopathyor cataract formation impairing the visionneeded to operate a motor vehicle, andneuropathy affecting the ability to feel footpetals can each impact driving safety (4).However, the incidence of these conditionsis not sufficiently extensive to justify re-striction of driving privileges for all driverswith diabetes. Driving mishaps related todiabetes are relatively infrequent for mostdrivers with diabetes and occur at a lowerrate than mishaps of many other driverswith conditions that affect driving perfor-mance and that are tolerated by society.

However, just as there are some pa-tients with conditions that increase their

risk of incurring driving mishaps, such asunstable coronary heart disease, obstruc-tive sleep apnea, epilepsy, Parkinson’sdisease, or alcohol and substance abuse,there are also some drivers with diabetesthat have a higher risk for driving mis-haps. The challenges are to identify high-risk individuals and develop measures toassist them to lower their risk for drivingmishaps.

Understanding the risk of diabetesand drivingIn a recent Scottish study, only 62% ofhealth care professionals suggested thatinsulin-treated drivers should test theirblood glucose before driving; 13% of healthcare professionals thought it safe to drivewith blood glucose,72mg/dL (4mmol/L),and 8% did not know that impaired aware-ness of hypoglycemia might be a contrain-dication to driving (5). It is important thathealth care professionals be knowledgeableand take the lead in discussing risk reduc-tion for their patients at risk for hypoglyce-mia. In a large international study, nearlyhalf of drivers with type 1 diabetes andthree-quarters of those with type 2 diabeteshad never discussed driving guidelines withtheir physician (8).

A meta-analysis of 15 studies sug-gested that the relative risk of having amotor vehicle accident for people withdiabetes as a whole, i.e., without differen-tiating those with a significant risk fromthose with little or no risk, as comparedwith the general population ranges be-tween 1.126 and 1.19, a 12–19% in-creased risk (6). Some published studiesindicated that drivers with type 1 diabeteshave a slightly higher risk, with a relativerisk ratio of ;2 (7,8,9), but this was notconfirmed by other studies (10). Two stud-ies even suggested that there is no increasedrisk associated with insulin-treated diabe-tes (11,12), but the methodologies usedhave been criticized (13).

This increased risk of collisions mustbe interpreted in the light of society’s tol-erance of other and much higher–riskconditions. For example, 16-year-oldmales have 42 times more collisions than35- to 45-year-old women. If the heaviestcar collides with the lightest car, the driverof the latter is 20 times more likely to bekilled than the driver of the former. Themost dangerous rural highways are 9.2times more dangerous than the safest urbanhighways. Driving at 1:00 A.M. on Sunday is142 times more dangerous than driving at11:00 A.M. (7). Driverswith attention deficit/hyperactivity disorder have a relative risk

ratio of;4 (14), whereas those with sleepapnea have a relative risk of ;2.4 (15). Ifsociety tolerates these conditions, it wouldbe unjustified to restrict the driving priv-ileges of an entire class of individuals whoare at much lower risk, such as driverswith diabetes.

The most significant subgroup ofpersons with diabetes for whom a greaterdegree of restrictions is often applied isdrivers managing their diabetes with in-sulin. Yet, when the type of diabetes iscontrolled for, insulin therapy per se hasnot been found to be associated with in-creased driving risk (3,16,17). While im-paired awareness of hypoglycemia hasbeen found to relate to increased incidenceof motor vehicle crashes in some studies(12), it has not been found to be a relevantvariable in other studies (4,7,23). The sin-gle most significant factor associated withdriving collisions for drivers with diabetesappears to be a recent history of severe hy-poglycemia, regardless of the type of diabe-tes or the treatment used (1,3,18–21).

The American Diabetes AssociationWorkgroup on Hypoglycemia defined se-vere hypoglycemia as low blood glucoseresulting in neuroglycopenia that disruptscognitive motor function and requires theassistance of another to actively administercarbohydrate, glucagon, or other resuscita-tive actions (22). In a prospective multicen-ter study of 452 drivers with type 1 diabetesfollowed monthly for 12 months, 185 par-ticipants (41%) reported a total of 503 epi-sodes of moderate hypoglycemia (wherethe driver could still treat him/herself butcould no longer drive safely) and 23 partic-ipants (5%) reported 31 episodes of severehypoglycemia (where the driver was unableto treat him/herself) while driving (21).Conversely, the Diabetes Control andCom-plications Trial (DCCT) group reported 11motor vehicle accidents in 714 episodes ofsevere hypoglycemia, a rate of 1.5% (23).

The significant impact of moderatehypoglycemia while driving is supportedby multiple studies demonstrating thatmoderate hypoglycemia significantly andconsistently impairs driving safety (24–26)and judgment (27,28) as towhether to con-tinue to drive or to self-treat (29,30) undersuch metabolic conditions. In one study,25% of respondents thought it was safe todrive even when blood glucose was ,70mg/dL (3.9 mmol/L) (31).

While significant hyperglycemia mayimpair cognitive, motor, and perceptualfunctioning (32–35), there is only one re-port suggesting extreme hyperglycemiacan impact driving safety (36). Thus,


Position statement

efforts to equate hyperglycemia with driv-ing impairment are currently not scientif-ically justified.

Individual differencesEighty percent of episodes of severe hy-poglycemia affect about 20% of peoplewith type 1 diabetes (37–39). Availabledata suggest that a small subgroup of driv-ers with type 1 diabetes account for themajority of hypoglycemia-related colli-sions (9,30,40). When 452 drivers withtype 1 diabetes were followed prospec-tively for a year, baseline reports of priorepisodes of mild symptomatic hypoglyce-mia while driving or severe hypoglycemiawhile driving, hypoglycemia-related driv-ing mishaps, or hypoglycemia-relatedcollisions were associated with a higherrisk of driving mishaps in the following12 months by 3, 6, 6, and 20%, respec-tively. Risk increased exponentially withadditional reported episodes: If individu-als had two episodes of severe hypoglyce-mia in the preceding 12 months their riskincreased to 12%, and two collisions inthe previous 2 years increased their riskby 40%. The strongest predictors in-volved a history of hypoglycemia whiledriving (21). Laboratory studies that com-pared drivers with type 1 diabetes whohad no history of hypoglycemia-relateddriving mishap in the past year to thosewho had more than one mishap foundthat those with a history of mishaps: 1)drove significantly worse during progres-sive mild hypoglycemia (70–50 mg/dL,3.9–2.8 mmol/L) but drove equally wellwhen blood glucose was normal (euglyce-mia); 2) had a lower epinephrine responsewhile driving during hypoglycemia, 3)were more insulin sensitive, and 4) demon-strated greater difficulties with workingmemory and information processing speedduring euglycemia and hypoglycemia(24,40,41). Thus, a history of mishapsshould be used as a basis for identifyinginsulin-managed drivers with elevatedrisk of future mishaps. Such individualsare appropriately subjected to additionalscreening requirements.

Four studies have demonstrated thatBlood Glucose Awareness Training(BGAT) reduces the occurrence of colli-sions and moving vehicle violations whileimproving judgment about whether todrive while hypoglycemic (42–45). BGATis an 8-week psycho-educational trainingprogram designed to assist individualswith type 1 diabetes to better anticipate,prevent, recognize, and treat extremeblood glucose events. This intervention

can be effectively delivered over the inter-net (46). Diabetes Driving (diabetesdriv-ing.com), a program funded by theNational Institutes of Health, is anotherinternet-based tool to help assess therisk of driving mishaps and assist high-risk drivers to avoid hypoglycemia whiledriving and to better detect and managehypoglycemia if it occurs while driving.

RECOMMENDATIONS

Identifying and evaluating diabetesin driversIndividuals whose diabetes poses a sig-nificantly elevated risk to safe drivingmust be identified and evaluated prior togetting behind the wheel. Because peoplewith diabetes are diverse in terms of thenature of their condition, the symptomsthey experience, and the measures theytake to manage their diabetes, it is impor-tant that identification and evaluation pro-cesses be appropriate, individualized, andbased not solely on a diagnosis of diabetesbut rather on concrete evidence of actualrisk. Laws that require all people withdiabetes (or all people with insulin-treateddiabetes) to be medically evaluated as acondition of licensure are ill advised be-cause they combine people with diabetesinto one group rather than identifyingthose drivers who may be at increased riskdue to potential difficulties in avoidinghypoglycemia or the presence of compli-cations. In addition, the logistics of regis-tering and evaluating millions of peoplewith diabetes who wish to drive presentsan enormous administrative and fiscal bur-den to licensing agencies. States that requiredrivers to identify diabetes should limitthe identification to reports of diabetes-related problems.

To identify potentially at-risk drivers, ashort questionnaire can be used to findthose drivers who may require furtherevaluation. The questionnaire should askwhether the driver has, within the past 12months, lost consciousness due to hypo-glycemia, experienced hypoglycemia thatrequired intervention from another per-son to treat or that interfered with driving,or experienced hypoglycemia that devel-oped without warning. The questionnaireshould also query about loss of visualacuity or peripheral vision and loss offeeling in the right foot. Inasmuch asobstructive sleep apnea is more commonin people with type 2 diabetes than in thenondiabetic population, patients shouldbe queried about falling asleep during theday. Any positive answer should trigger an

evaluation to determine whether restric-tions on the license or mechanical mod-ifications to the vehicle (e.g., handcontrols for people with an insensatefoot) are necessary to ensure public safety.It is ill-advised to determine risk fordriving mishaps based on a driver’s gly-cosylated hemoglobin because episodictransitions into hypoglycemia, not averageblood glucose, increases risk of drivingmishaps.

Evaluation of drivers with diabetesmust include an assessment by the treat-ing physician or another diabetes special-ist who can review recent diabetes historyand provide to the licensing agency arecommendation about whether thedriver has a condition that impairs hisor her ability to safely operate a motorvehicle. The treating physician or anotherphysician who is knowledgeable aboutdiabetes is the best source of informationconcerning the driver’s diabetes manage-ment and history. The input of such aphysician is essential to assess a person’sdiabetes management and determinewhether operation of a motor vehicle issafe and practicable. If questions ariseconcerning the safe driving ability of aperson with chronic complications of di-abetes (e.g., retinopathy or neuropathy),the individual should be referred to a spe-cialist with expertise in evaluating thediabetes-related problem for specific rec-ommendations.

Physicians should be requested toprovide the following information: 1)whether the driver has had an episode ofsevere hypoglycemia requiring interven-tion from another person within the pre-vious 2 years (and when this happened);2) whether there was an explanation forthe hypoglycemia; 3) whether the driver isat increased risk of severe hypoglycemia;4) whether the driver has the ability torecognize incipient hypoglycemia andknows how to take appropriate correctiveaction; 5) whether the driver provides ev-idence of sufficient self-monitoring ofblood glucose; 6) whether the driver hasany diabetes-related complications affect-ing safe driving that need further assess-ment; and 7) whether the driver has agood understanding of diabetes and itstreatment, has been educated on theavoidance of hypoglycemia while driving,and is willing to follow a suggested treat-ment plan.

When evaluating a driverwith a historyof severe hypoglycemia, impaired hypogly-cemia awareness, or a diabetes-related mo-tor vehicle accident, it is necessary to



investigate the reasons for the hypoglyce-mia and to determine whether it is afunction of the driver’s treatment regimenor lifestyle, a psychological reaction to themanagement of their diabetes, or the nor-mal course of diabetes. Appropriate clini-cal interventions should be instituted.

Licensing decisions followingevaluationDrivers with diabetes should only have alicense suspended or restricted if doing sois the only practical way to address anestablished safety risk. Licensing deci-sions should reflect deference to the pro-fessional judgment of the evaluatingphysician with regard to diabetes, whilealso balancing the licensing agency’s needto keep the roads and the public safe.States should have medical advisoryboards whose role is to assess potentialdriving risks based on continually up-dated medical information, to ensurethat licensing agency staff is prepared tohandle diabetes licensing issues, and tomake recommendations relevant to indi-vidual drivers. State medical advisoryboards should have representation byhealth care professionals with expertisein treating diabetes, in addition to the in-formation provided by the driver’s treatingphysician, prior to making licensing deci-sions for people with diabetes. Where themedical advisory board does not have apermanent member with expertise in di-abetes, such an expert should be consultedin cases involving restrictions on a driverwith diabetes.

As discussed above, a history of hy-poglycemia does not mean an individualcannot be a safe driver. Rather, whenthere is evidence of a history of severehypoglycemia, an appropriate evaluationshould be undertaken to determine thecause of the low blood glucose, the cir-cumstances of the episode, whether it wasan isolated incident, whether adjustmentto the insulin regimen may mitigate therisk, and the likelihood of such an episoderecurring. It is important that licensingdecisions take into consideration contrib-utory factors that may mitigate a potentialrisk, and that licensing agencies do notadopt a “one strike” approach to licensingpeople with diabetes. Drivers with diabe-tes must be individually assessed to deter-mine whether their diabetes poses a safetyrisk. The mere fact that a person’s diabeteshas come to the attention of the licensingagencydwhether by a report or becauseof an accidentdshould not itself pre-determine a licensing decision.

Generally, severe hypoglycemia thatoccurs during sleep should not disqualifya person from driving. Hypoglycemia thatoccurswhile theperson is not driving shouldbe examined to determine if it is indicativeof a larger problem or an event that is notlikely to recur while the person is behindthe wheel of a car (e.g., hypoglycemia thatoccurs during an intense bout of exercise).Some episodes of severe hypoglycemia canbe explained and corrected with the assis-tance of a diabetes health care professional,e.g., episodes that occur because of achange in medication. However, recurrentepisodes of severe hypoglycemia, definedas two or more episodes in a year, mayindicate that a person is not able to safelyoperate a motor vehicle.

States whose licensing rules lead to asuspension of a driver’s license followingan episode of hypoglycemia should allowfor waiver of these rules when the hypo-glycemia can be explained and addressedby the treating physician and is not likelyto recur. For example, waivers may be ap-propriate following hypoglycemia thathappens as a result of a change in medi-cation or during or concurrent with ill-ness or pregnancy. Licensing agenciesmay request documentation from thephysician attesting that the patient meetsthe conditions for a waiver (which mayinclude, among other requirements, edu-cation on diabetes management andavoidance of hypoglycemia).

Drivers with a suspended license be-cause of factors related to diabetes shouldbe eligible to have their driver’s license re-instated following a sufficient period oftime (usually no more than 6 months)upon advice from the treating physicianthat the driver has made appropriate ad-justments and is adhering to a regimenthat has resulted in correction of the prob-lems that led to the license suspension. Fol-lowing reinstatement of driving privileges,periodic follow-up evaluation is necessaryto ensure that the person remains safelyable to operate a motor vehicle.

People who experience progressiveimpairment of their awareness of hypo-glycemia should consult a health careprovider to determine whether it is safeto continue driving with proper measuresto avoid disruptive hypoglycemia (such astesting blood glucose before driving andat regular intervals in the course of ajourney lasting more than 30–60 min). Ifthe driver is able to make adjustments toimprove awareness or prevent disruptivehypoglycemia while driving, there shouldnot be license restrictions. Continuous

glucose monitoring may also be beneficial,particularly when noting the direction ofthe glucose trend. If this technology isused, the person using the device needsto appreciate that any action taken (e.g.,additional carbohydrate consumption)needs to be based on a blood glucose mea-surement.

The determination of which disquali-fied drivers should be reevaluated andwhen this should be done should bemadeon an individual basis considering factorssuch as the circumstances of the disqual-ifying event and changes in medicationand behavior that have been implementedby the driver. When an assessment deter-mines that the driver should be evaluatedat some point in the future, the driver’sphysician should be consulted to deter-mine the length of the reevaluation pe-riod. A driver with diabetes should notbe kept in an endless cycle of reevaluationif there is no longer a significantly ele-vated safety risk.

The determination of medical fitnessto drive should be a clinical one, weighingthe various factors noted above. Decisionsabout whether licensing restrictions arenecessary to ensure safety of the travelingpublic are ultimately determined by thelicensing agency, taking into account theclinical determination of medical fitness.

Physician reportingAlthough the concept behind mandatoryphysician reporting laws is to keep roadssafe by eliminating unacceptable riskfrom impaired driving, such laws havethe unintended consequence of discour-aging people with diabetes from discus-sing their condition frankly with aphysician when there is a problem thatneeds correction due to fear of losing theirlicense. Patients who are not candid withtheir physicians are likely to receive in-ferior treatment and therefore may expe-rience complications that present adriving risk. In addition to the negativeeffect that mandatory reporting has on thephysician-patient relationship, there isno evidence that mandatory physicianreporting reduces the crash rate or im-proves public safety (47).

Physicians should be permitted toexercise professional judgment in decid-ing whether and when to report a patientto the licensing agency for review ofdriving privileges. States that allow physi-cians to make such reports should focusonwhether the driver’s mental or physicalcondition impairs the patient’s ability toexercise safe control over a motor vehicle.


Position statement

Reports based solely on a diagnosis of di-abetes, or tied to a characterization thatthe driver has a condition involving lapsesof consciousness, are too broad and donot adequately measure individual risk.Ultimately, reports must be left to the dis-cretion of the physician, using profes-sional judgment about whether thepatient poses a safety risk. Further, in or-der to protect the physician-patient rela-tionship and ensure the open and honestcommunication that ultimately promotessafety, it is important that physicians beimmunized from liability, both for mak-ing reports and not making reports.

Patient education and clinicalinterventionsIt is important that health care professio-nals be knowledgeable and take the lead indiscussing risk reduction for their patientsat risk for disruptive hypoglycemia. Thisstarts with health care professionals beingconversant with safe practices, particularlyfor those patients at increased risk fordiabetes-related incidents. Perhaps themost important aspect of encouraging peo-ple with diabetes to be safe drivers is forhealth care professionals who treat diabeticdrivers to provide education about drivingwith diabetes and potential risks associatedwith patients’ treatment regimens. Whenthat regimen includes the possibility of hy-poglycemia, education should include in-struction on avoiding and responding tohypoglycemia, discussion about the pa-tient’s vulnerability for driving mishaps,and ongoing learning to ensure that pa-tients have knowledge of when it is and isnot safe for them to drive. For example, therisks of driving under the influence of alco-hol are well known, but the delayed hypo-glycemic effects of even moderate alcoholintake are not, and alcohol exacerbates thecognitive impairment associated with hy-poglycemia (48). Inasmuch as hypoglyce-mia can be mistaken for intoxication, andboth increase the risk of motor vehicle ac-cidents, patients should be counseled totest glucose more frequently for severalhours after moderate alcohol intake.When a patient has complications of dia-betes, it is important for the physician todiscuss with the driver the effect of thosecomplications, if any, on driving ability.

Physicians and other health care pro-fessionals who treat people with diabetesshould regularly discuss the risk of drivingwith low blood glucose with their patients.Clinical visits should include review ofblood glucose logs and questions to thepatient about symptoms associated with

high or low blood glucose levels and whatthe patient did to treat those levels. Allow-ing health care professionals to exerciseprofessional judgment about the informa-tion they learn in these patient conversa-tions will encourage candid sharing ofinformation and lead to improved patienthealth and road safety.

Clinical interventions in response tohypoglycemia vary by individual but mayinclude strategies for the frequency andtiming of blood glucose monitoring,medication dosage changes, and estab-lishing more conservative glucose targetsif there is a history of severe hypo-glycemia. Certain people who have ahistory of severe hypoglycemia may beencouraged by their health care providerto use continuous glucose monitoringsystems that enable them to detect atrend toward hypoglycemia before glu-cose levels fall to a level that will affectsafe driving.

Of note, special care should be taken toprevent hypoglycemia while operating anyvehicle in driverswith type 1 diabetes and inthosewith type 2 diabeteswho are at risk fordeveloping hypoglycemia. They should beinstructed to always check blood glucosebefore getting behind the wheel and atregular intervals while driving for periodsof 1 h or greater. Consideration should begiven to factors that may predict a fall inblood glucose, including time of insulinadministration, timing of the last meal orfood ingestion, and exercise type, duration,intensity, and timing. Low blood glucosevalues should be treated immediately andappropriately, and the driver should notdrive until blood glucose is in a safelyacceptable range, usually after 30–60min because of delayed recovery of cog-nitive function.

People with diabetes who are at riskfor disruptive hypoglycemia should becounseled to: 1) always carry a blood glu-cose meter and appropriate snacks,including a quick-acting source of sugar(such as juice, nondiet soda, hard candy,or dextrose tablets) as well as snacks withcomplex carbohydrate, fat, and protein(e.g., cheese crackers), in their vehicle;2) never begin an extended drive withlow normal blood glucose (e.g., 70–90mg/dL) without prophylactic carbohy-drate consumption to avoid a fall in bloodglucose during the drive; 3) stop the ve-hicle as soon any of the symptoms of lowblood glucose are experienced and mea-sure and treat the blood glucose level; and4) not resume driving until their bloodglucose and cognition have recovered.

CONCLUSIONdIn summary, peoplewith diabetes should be assessed individ-ually, taking into account each individu-al’s medical history as well as the potentialrelated risks associated with driving.

AcknowledgmentsdThe American DiabetesAssociation thanks the members of the writinggroup for developing this statement: DanielLorber,MD,FACP,CDE (Chair); JohnAnderson,MD;ShereenArent, JD;Daniel J. Cox, PhD,ABPP;BrianM.Frier, BSc,MD,FRCPE,FRCPG;MichaelA. Greene, JD; John W. Griffin, Jr., JD; GaryGross, JD; Katie Hathaway, JD; Irl Hirsch, MD;Daniel B. Kohrman, JD; David G. Marrero, PhD;Thomas J. Songer, PhD; and Alan L. Yatvin, JD.

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Position statement

DiabetesManagement in CorrectionalInstitutionsAMERICAN DIABETES ASSOCIATION

A t any given time, over 2 million peo-ple are incarcerated in prisons andjails in the U.S (1). It is estimated

that nearly 80,000 of these inmates havediabetes, a prevalence of 4.8% (2). In ad-dition, many more people pass throughthe corrections system in a given year. In1998 alone, over 11 million people werereleased from prison to the community(1). The current estimated prevalence ofdiabetes in correctional institutions issomewhat lower than the overall U.S. prev-alence of diabetes, perhaps because the in-carcerated population is younger than thegeneral population. The prevalence of di-abetes and its related comorbidities andcomplications, however, will continue toincrease in the prison population as currentsentencing guidelines continue to increasethe number of aging prisoners and the in-cidence of diabetes in young people con-tinues to increase.

People with diabetes in correctionalfacilities should receive care that meetsnational standards. Correctional institu-tions have unique circumstances thatneed to be considered so that all standardsof care may be achieved (3). Correctionalinstitutions should have written policiesand procedures for the management ofdiabetes and for training of medical andcorrectional staff in diabetes care practices.These policies must take into considerationissues such as security needs, transfer fromone facility to another, and access to med-ical personnel and equipment, so that allappropriate levels of care are provided. Ide-ally, these policies should encourage or atleast allow patients to self-manage their di-abetes. Ultimately, diabetes management isdependent upon having access to neededmedical personnel and equipment. Ongo-ing diabetes therapy is important in orderto reduce the risk of later complications,including cardiovascular events, visual

loss, renal failure, and amputation. Earlyidentification and intervention for peoplewith diabetes is also likely to reduceshort-term risks for acute complications re-quiring transfer out of the facility, thus im-proving security.

This document provides a general setof guidelines for diabetes care in correc-tional institutions. It is not designed to be adiabetes management manual. More de-tailed information on the management ofdiabetes and related disorders can be foundin the American Diabetes Association(ADA)Clinical Practice Recommendations,published each year in January as the firstsupplement to Diabetes Care, as well as the“Standards ofMedical Care in Diabetes” (4)contained therein. This discussion will fo-cus on those areas where the care of peoplewith diabetes in correctional facilities maydiffer, and specific recommendations aremade at the end of each section.

INTAKE MEDICALASSESSMENT

Reception screeningReception screening should emphasizepatient safety. In particular, rapid identi-fication of all insulin-treated persons withdiabetes is essential in order to identifythose at highest risk for hypo- and hyper-glycemia and diabetic ketoacidosis(DKA). All insulin-treated patients shouldhave a capillary blood glucose (CBG)determination within 1–2 h of arrival.Signs and symptoms of hypo- or hyper-glycemia can often be confused with in-toxication or withdrawal from drugs oralcohol. Individuals with diabetes exhib-iting signs and symptoms consistent withhypoglycemia, particularly altered mentalstatus, agitation, combativeness, and dia-phoresis, should have finger-stick bloodglucose levels measured immediately.

Intake screeningPatients with a diagnosis of diabetesshould have a complete medical historyand physical examination by a licensedhealth care provider with prescriptive au-thority in a timely manner. If one is notavailable on site, one should be consultedby those performing reception screening.The purposes of this history and physicalexamination are to determine the type ofdiabetes, current therapy, alcohol use, andbehavioral health issues, aswell as to screenfor the presence of diabetes-related com-plications. The evaluation should reviewthe previous treatment and the past historyof both glycemic control and diabetescomplications. It is essential that medica-tion and medical nutrition therapy (MNT)be continued without interruption uponentry into the correctional system, as ahiatus in either medication or appropriatenutritionmay lead to either severe hypo- orhyperglycemia that can rapidly progress toirreversible complications, even death.

Intake physical examination andlaboratoryAll potential elements of the initial med-ical evaluation are included in Table 5 ofthe ADA’s “Standards of Medical Care inDiabetes,” referred to hereafter as the“Standards of Care” (4). The essentialcomponents of the initial history andphysical examination are detailed in Fig.1. Referrals should be made immediatelyif the patient with diabetes is pregnant.

Recommendationsc Patients with a diagnosis of diabetesshould have a completemedical historyand undergo an intake physical exam-ination by a licensed health pro-fessional in a timely manner. (E)

c Insulin-treated patients should have aCBG determination within 1–2 h ofarrival. (E)

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

SCREENING FOR DIABETESdConsistent with the ADA Standards ofCare, patients should be evaluated fordiabetes risk factors at the intake physicaland at appropriate times thereafter. Those


Originally approved 1989. Most recent revision, 2008.Abbreviations:CBG, capillary blood glucose; DKA, diabetic ketoacidosis; GDM, gestational diabetes mellitus;

MNT, medical nutrition therapy.DOI: 10.2337/dc12-s087© 2012 by the American Diabetes Association. Readers may use this article as long as the work is properly




who are at high risk should be consideredfor blood glucose screening. If pregnant, arisk assessment for gestational diabetesmellitus (GDM) should be undertaken atthe first prenatal visit. Patients with clin-ical characteristics consistent with a highrisk for GDM should undergo glucosetesting as soon as possible. High-riskwomen not found to have GDM at theinitial screening and average-risk womenshould be tested between 24 and 28weeks of gestation. For more detailedinformation on screening for both type 2and gestational diabetes, see the ADAPosition Statement “Screening for Type2 Diabetes” (5) and the Standards ofCare (4).

MANAGEMENT PLANdGlycemiccontrol is fundamental to the manage-ment of diabetes. A management plan toachieve normal or near-normal glycemiawith an A1C goal of ,7% should be de-veloped for diabetes management at thetime of initial medical evaluation. Goalsshould be individualized (4), and less strin-gent treatment goalsmay be appropriate forpatients with a history of severe hypoglyce-mia, patients with limited life expectancies,

elderly adults, and individuals with co-morbid conditions (4). This plan shouldbe documented in the patient’s recordand communicated to all persons in-volved in his/her care, including securitystaff. Table 1, taken from the ADA Stand-ards of Care, provides a summary of rec-ommendations for setting glycemiccontrol goals for adults with diabetes.

People with diabetes should ideallyreceive medical care from a physician-coordinated team. Such teams include,but are not limited to, physicians, nurses,dietitians, and mental health professio-nals with expertise and a special interestin diabetes. It is essential in this collabo-rative and integrated team approach thatindividuals with diabetes assume asactive a role in their care as possible.Diabetes self-management education is anintegral component of care. Patient self-management should be emphasized, andthe plan should encourage the involve-ment of the patient in problem solving asmuch as possible.

It is helpful to house insulin-treatedpatients in a common unit, if this ispossible, safe, and consistent with pro-viding access to other programs at the

correctional institution. Common hous-ing not only can facilitate mealtimes andmedication administration, but also po-tentially provides an opportunity for di-abetes self-management education to bereinforced by fellow patients.

NUTRITION AND FOODSERVICESdNutrition counseling andmenu planning are an integral part of themultidisciplinary approach to diabetesmanagement in correctional facilities. Acombination of education, interdisciplin-ary communication, and monitoring foodintake aids patients in understandingtheir medical nutritional needs and canfacilitate diabetes control during and afterincarceration.

Nutrition counseling for patientswith diabetes is considered an essentialcomponent of diabetes self-management.People with diabetes should receive indi-vidualized MNT as needed to achievetreatment goals, preferably provided by aregistered dietitian familiar with the com-ponents of MNT for persons with diabetes.

Educating the patient, individually orin a group setting, about how carbohy-drates and food choices directly affect

Figure 1dEssential components of the initial history and physical examination. Alb/Cr ratio, albumin-to-creatinine ratio; ALT, alanine amino-transferase; AST, aspartate aminotransferase.


Correctional Institutions

diabetes control is the first step in facili-tating self-management. This educationenables the patient to identify better foodselections from those available in thedining hall and commissary. Such anapproach is more realistic in a facilitywhere the patient has the opportunity tomake food choices.

The easiest and most cost-effectivemeans to facilitate good outcomes in pa-tients with diabetes is instituting a heart-healthy diet as the master menu (6). Thereshould be consistent carbohydrate contentat each meal, as well as a means to identifythe carbohydrate content of each food se-lection. Providing carbohydrate content offood selections and/or providing educationin assessing carbohydrate content enablespatients to meet the requirements of theirindividual MNT goals. Commissariesshould also help in dietary managementby offering healthy choices and listing thecarbohydrate content of foods.

The use of insulin or oral medicationsmay necessitate snacks in order to avoidhypoglycemia. These snacks are a part ofsuch patients’ medical treatment plansand should be prescribed bymedical staff.

Timing of meals and snacks must becoordinated with medication administra-tion as needed to minimize the risk ofhypoglycemia, as discussed more fully inthe MEDICATION section of this document.For further information, see the ADA Po-sition Statement “Nutrition Principlesand Recommendations in Diabetes” (7).

URGENT AND EMERGENCYISSUESdAll patients must have accessto prompt treatment of hypo- and hyper-glycemia. Correctional staff should betrained in the recognition and treatmentof hypo- and hyperglycemia, and appro-

priate staff should be trained to adminis-ter glucagon. After such emergency care,patients should be referred for appropri-ate medical care to minimize risk of futuredecompensation.

Institutions should implement a pol-icy requiring staff to notify a physician ofall CBG results outside of a specifiedrange, as determined by the treatingphysician (e.g., ,50 or .350 mg/dl).

HyperglycemiaSevere hyperglycemia in a person withdiabetes may be the result of intercurrentillness, missed or inadequate medication,or corticosteroid therapy. Correctionalinstitutions should have systems in placeto identify and refer to medical staff allpatients with consistently elevated bloodglucose as well as intercurrent illness.

The stress of illness in those with type1 diabetes frequently aggravates glycemiccontrol and necessitates more frequentmonitoring of blood glucose (e.g., every4–6 h). Marked hyperglycemia requirestemporary adjustment of the treatmentprogram and, if accompanied by ketosis,interaction with the diabetes care team.Adequate fluid and caloric intake mustbe ensured. Nausea or vomiting accom-panied with hyperglycemia may indicateDKA, a life-threatening condition that re-quires immediate medical care to preventcomplications and death. Correctional in-stitutions should identify patients withtype 1 diabetes who are at risk for DKA,particularly those with a prior history offrequent episodes of DKA. For further in-formation see “Hyperglycemic Crisis inDiabetes” (8).

HypoglycemiaHypoglycemia is defined as a blood glu-cose level ,70 mg/dl. Severe hypoglyce-mia is a medical emergency defined ashypoglycemia requiring assistance of athird party and is often associated withmental status changes that may includeconfusion, incoherence, combativeness,somnolence, lethargy, seizures, or coma.Signs and symptoms of severe hypogly-cemia can be confused with intoxicationor withdrawal. Individuals with diabetesexhibiting signs and symptoms consistentwith hypoglycemia, particularly alteredmental status, agitation, and diaphoresis,should have their CBG levels checkedimmediately.

Security staff who supervise patientsat risk for hypoglycemia (i.e., those oninsulin or oral hypoglycemic agents)should be educated in the emergency re-

sponse protocol for recognition and treat-ment of hypoglycemia. Every attemptshould be made to document CBG beforetreatment. Patients must have immediateaccess to glucose tablets or other glucose-containing foods. Hypoglycemia can gen-erally be treated by the patient with oralcarbohydrates. If the patient cannot berelied on to keep hypoglycemia treatmenton his/her person, staff members shouldhave ready access to glucose tablets orequivalent. In general, 15–20 g oral glu-cose will be adequate to treat hypoglyce-mic events. CBG and treatment should berepeated at 15-min intervals until bloodglucose levels return to normal (.70 mg/dl).

Staff should have glucagon for intra-muscular injection or glucose for intra-venous infusion available to treat severehypoglycemia without requiring trans-port of the hypoglycemic patient to anoutside facility. Any episode of severehypoglycemia or recurrent episodes ofmild to moderate hypoglycemia requirereevaluation of the diabetes managementplan by the medical staff. In certain casesof unexplained or recurrent severe hypo-glycemia, it may be appropriate to admitthe patient to the medical unit for obser-vation and stabilization of diabetes man-agement.

Correctional institutions should havesystems in place to identify the patients atgreater risk for hypoglycemia (i.e., thoseon insulin or sulfonylurea therapy) and toensure the early detection and treatmentof hypoglycemia. If possible, patients atgreater risk of severe hypoglycemia (e.g.,those with a prior episode of severehypoglycemia) may be housed in unitscloser to the medical unit in order tominimize delay in treatment.

Recommendationsc Train correctional staff in the recogni-tion, treatment, and appropriate re-ferral for hypo- and hyperglycemia. (E)

c Train appropriate staff to administerglucagon. (E)

c Train staff to recognize symptoms andsigns of serious metabolic decompensa-tion, and immediately refer the patientfor appropriate medical care. (E)

c Institutions should implement a policyrequiring staff to notify a physician ofall CBG results outside of a specifiedrange, as determined by the treatingphysician (e.g., ,50 or .350 mg/dl).(E)

c Identify patients with type 1 diabeteswho are at high risk for DKA. (E)

Table 1dSummary of recommendations forglycemic, 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/lifeexpectancy, comorbid conditions, known CVD oradvancedmicrovascular complications, hypoglycemiaunawareness, individual and patient considerations.†Based on patient characteristics and response totherapy, higher or lower SBP targets may be appro-priate. ‡In individuals with overt CVD, a lower LDLcholesterol goal of ,70 mg/dL (1.8 mmol/L), usinga high dose of a statin, is an option.


MEDICATIONdFormularies shouldprovide access to usual and customaryoral medications and insulins necessary totreat diabetes and related conditions.While not every brand name of insulinand oral medication needs to be available,individual patient care requires access toshort-, medium-, and long-acting insulinsand the various classes of oral medica-tions (e.g., insulin secretagogues, bigua-nides, a-glucosidase inhibitors, andthiazolidinediones) necessary for currentdiabetes management.

Patients at all levels of custody shouldhave access to medication at dosing fre-quencies that are consistent with theirtreatment plan and medical direction. Iffeasible and consistent with security con-cerns, patients on multiple doses of short-acting oral medications should be placedin a “keep on person” program. In othersituations, patients should be permittedto self-inject insulin when consistentwith security needs. Medical departmentnurses should determine whether patientshave the necessary skill and responsible be-havior to be allowed self-administrationand the degree of supervision necessary.When needed, this skill should be a partof patient education. Reasonable syringecontrol systems should be established.

In the past, the recommendation thatregular insulin be injected 30–45 min be-fore meals presented a significant prob-lem when “lock downs” or otherdisruptions to the normal schedule ofmeals and medications occurred. Theuse of multiple-dose insulin regimens us-ing rapid-acting analogs can decrease thedisruption caused by such changes inschedule. Correctional institutionsshould have systems in place to ensurethat rapid-acting insulin analogs andoral agents are given immediately beforemeals if this is part of the patient’s medicalplan. It should be noted however thateven modest delays in meal consumptionwith these agents can be associated withhypoglycemia. If consistent access to foodwithin 10 min cannot be ensured, rapid-acting insulin analogs and oral agents areapproved for administration during orimmediately after meals. Should circum-stances arise that delay patient access toregular meals following medication ad-ministration, policies and proceduresmust be implemented to ensure the pa-tient receives appropriate nutrition toprevent hypoglycemia.

Both continuous subcutaneous insu-lin infusion and multiple daily insulininjection therapy (consisting of three or

more injections a day) can be effectivemeans of implementing intensive diabetesmanagement with the goal of achievingnear-normal levels of blood glucose (9).While the use of these modalities may bedifficult in correctional institutions, everyeffort should be made to continue multi-ple daily insulin injection or continuoussubcutaneous insulin infusion in peoplewho were using this therapy before incar-ceration or to institute these therapies asindicated in order to achieve blood glu-cose targets.

It is essential that transport of patientsfrom jails or prisons to off-site appoint-ments, such as medical visits or courtappearances, does not cause significantdisruption in medication or meal timing.Correctional institutions and police lock-ups should implement policies and pro-cedures to diminish the risk of hypo- andhyperglycemia by, for example, providingcarry-along meals and medication forpatients traveling to off-site appointmentsor changing the insulin regimen for thatday. The availability of prefilled insulin“pens” provides an alternative for off-siteinsulin delivery.

Recommendations

c Formularies should provide access tousual and customary oral medicationsand insulins to treat diabetes and re-lated conditions. (E)

c Patients should have access to medi-cation at dosing frequencies that areconsistent with their treatment planand medical direction. (E)

c Correctional institutions and policelock-ups should implement policiesand procedures to diminish the risk ofhypo- and hyperglycemia during off-site travel (e.g., court appearances). (E)

ROUTINE SCREENING FOR ANDMANAGEMENT OF DIABETESCOMPLICATIONSdAll patientswith a diagnosis of diabetes should re-ceive routine screening for diabetes-relatedcomplications, as detailed in the ADAStandards of Care (4). Interval chronicdisease clinics for persons with diabetesprovide an efficient mechanism to monitorpatients for complications of diabetes. Inthis way, appropriate referrals to consul-tant specialists, such as optometrists/ophthalmologists, nephrologists, andcardiologists, can be made on an as-neededbasis and interval laboratory testing canbe done.

The following complications shouldbe considered.

c Foot care: Recommendations for footcare for patients with diabetes and nohistory of an open foot lesion are de-scribed in the ADA Standards of Care.A comprehensive foot examination isrecommended annually for all patientswith diabetes to identify risk factorspredictive of ulcers and amputations.Persons with an insensate foot, an openfoot lesion, or a history of such a lesionshould be referred for evaluation by anappropriate licensed health professional(e.g., podiatrist or vascular surgeon).Special shoes should be provided asrecommended by licensed health pro-fessionals to aid healing of foot lesionsand to prevent development of newlesions.

c Retinopathy: Annual retinal examina-tions by a licensed eye care professionalshould be performed for all patientswith diabetes, as recommended in theADA Standards of Care. Visual changesthat cannot be accounted for by acutechanges in glycemic control requireprompt evaluation by an eye care pro-fessional.

c Nephropathy: An annual spot urinetest for determination of microalbumin-to-creatinine ratio should be performed.The use of ACE inhibitors or angiotensinreceptor blockers is recommended forall patients with albuminuria. Bloodpressure should be controlled to ,130/80 mmHg.

c Cardiac: People with type 2 diabetesare at a particularly high risk of coro-nary artery disease. Cardiovasculardisease risk factor management is ofdemonstrated benefit in reducing thiscomplication in patients with diabetes.Blood pressure should be measured atevery routine diabetes visit. In adultpatients, test for lipid disorders at leastannually and as needed to achieve goalswith treatment. Use aspirin therapy(75–162 mg/day) in all adult patientswith diabetes and cardiovascular riskfactors or known macrovascular dis-ease. Current national standards foradults with diabetes call for treatmentof lipids to goals of LDL #100, HDL.40, triglycerides ,150 mg/dl andblood pressure to a level of ,130/80mmHg.

MONITORING/TESTS OFGLYCEMIAdMonitoring of CBG is astrategy that allows caregivers and people



with diabetes to evaluate diabetes man-agement regimens. The frequency ofmonitoring will vary by patients’ glycemiccontrol and diabetes regimens. Patientswith type 1 diabetes are at risk for hypo-glycemia and should have their CBGmonitored three or more times daily. Pa-tients with type 2 diabetes on insulin needto monitor at least once daily and morefrequently based on their medical plan.Patients treated with oral agents shouldhave CBG monitored with sufficient fre-quency to facilitate the goals of glycemiccontrol, assuming that there is a programfor medical review of these data on anongoing basis to drive changes in medica-tions. Patients whose diabetes is poorlycontrolled or whose therapy is changingshould have more frequent monitoring.Unexplained hyperglycemia in a patientwith type 1 diabetes may suggest impend-ing DKA, and monitoring of ketonesshould therefore be performed.

Glycated hemoglobin (A1C) is a mea-sure of long-term (2- to 3-month) glyce-mic control. Perform the A1C test at leasttwo times a year in patients who aremeeting treatment goals (and who havestable glycemic control) and quarterly inpatients whose therapy has changed orwho are not meeting glycemic goals.

Discrepancies between CBGmonitor-ing results and A1C may indicate a he-moglobinopathy, hemolysis, or need forevaluation of CBG monitoring techniqueand equipment or initiation of morefrequent CBG monitoring to identifywhen glycemic excursions are occurringand which facet of the diabetes regimen ischanging.

In the correctional setting, policiesand procedures need to be developed andimplemented regarding CBG monitoringthat address the following.

c infection controlc education of staff and patientsc proper choice of meterc disposal of testing lancetsc quality control programsc access to health servicesc size of the blood samplec patient performance skillsc documentation and interpretation oftest results

c availability of test results for the healthcare provider (10)

Recommendationsc In the correctional setting, policies andprocedures need to be developed and

implemented to enable CBGmonitoringto occur at the frequency necessitated bythe individual patient’s glycemic controland diabetes regimen. (E)

c A1C should be checked every 3–6months. (E)

SELF-MANAGEMENTEDUCATIONdSelf-management ed-ucation is the cornerstone of treatmentfor all people with diabetes. The healthstaff must advocate for patients to partic-ipate in self-management as much aspossible. Individuals with diabetes wholearn self-management skills and makelifestyle changes can more effectivelymanage their diabetes and avoid or delaycomplications associated with diabetes.In the development of a diabetes self-management education program in thecorrectional environment, the unique cir-cumstances of the patient should beconsidered while still providing, to thegreatest extent possible, the elementsof the “National Standards for DiabetesSelf-Management Education” (11). Astaged approach may be used depend-ing on the needs assessment and thelength of incarceration. Table 2 setsout the major components of diabetesself-management education. Survivalskills should be addressed as soon aspossible; other aspects of educationmay be provided as part of an ongoingeducation program.

Ideally, self-management education iscoordinated by a certified diabetes edu-cator who works with the facility to de-velop polices, procedures, and protocolsto ensure that nationally recognized edu-cation guidelines are implemented. Theeducator is also able to identify patientswho need diabetes self-management ed-ucation, including an assessment of thepatients’ medical, social, and diabeteshistories; diabetes knowledge, skills, andbehaviors; and readiness to change.

STAFF EDUCATIONdPolicies andprocedures should be implemented toensure that the health care staff hasadequate knowledge and skills to directthe management and education of per-sons with diabetes. The health care staffneeds to be involved in the developmentof the correctional officers’ training pro-gram. The staff education programshould be at a lay level. Training shouldbe offered at least biannually, and thecurriculum should cover the following.

c what diabetes isc signs and symptoms of diabetesc risk factorsc signs and symptoms of, and emergencyresponse to, hypo- and hyperglycemia

c glucose monitoringc medicationsc exercisec nutrition issues including timing ofmeals and access to snacks

Recommendationsc Include diabetes in correctional staffeducation programs. (E)

ALCOHOL AND DRUGSdPatientswith diabetes who are withdrawing fromdrugs and alcohol need special consider-ation. This issue particularly affects initialpolice custody and jails. At an intakefacility, proper initial identification andassessment of these patients are critical.The presence of diabetes may complicatedetoxification. Patients in need of com-plicated detoxification should be referredto a facility equipped to deal with high-risk detoxification. Patients with diabetesshould be educated in the risks involvedwith smoking. All inmates should beadvised not to smoke. Assistance insmoking cessation should be providedas practical.

TRANSFER ANDDISCHARGEdPatients in jails may behoused for a short period of time beforebeing transferred or released, and it is notunusual for patients in prison to be trans-ferred within the system several timesduring their incarceration.One of themanychallenges that health care providers faceworking in the correctional system is howto best collect and communicate importanthealth care information in a timely mannerwhen a patient is in initial police custody, isjailed short term, or is transferred fromfacility to facility. The importance of thiscommunication becomes critical when thepatient has a chronic illness such as di-abetes.

Transferring a patient with diabetesfrom one correctional facility to anotherrequires a coordinated effort. To facilitate athorough review of medical informationand completion of a transfer summary, it iscritical for custody personnel to providemedical staff with sufficient notice beforemovement of the patient.

Before the transfer, the health carestaff should review the patient’s medicalrecord and complete a medical transfer


summary that includes the patient’s cur-rent health care issues. At a minimum, thesummary should include the following.

c the patient’s current medicationschedule and dosages

c the date and time of the last medicationadministration

c any recent monitoring results (e.g.,CBG and A1C)

c other factors that indicate a need forimmediate treatment ormanagement atthe receiving facility (e.g., recent epi-sodes of hypoglycemia, history of se-vere hypoglycemia or frequent DKA,concurrent illnesses, presence of di-abetes complications)

c information on scheduled treatment/appointments if the receiving facility isresponsible for transporting the patientto that appointment

c name and telephone/fax number of acontact person at the transferring fa-cility who can provide additional in-formation, if needed

Themedical transfer summary, whichacts as a quick medical reference for thereceiving facility, should be transferredalong with the patient. To supplement theflow of information and to increase theprobability that medications are correctlyidentified at the receiving institution,sending institutions are encouraged toprovide each patient with a medicationcard to be carried by the patient thatcontains information concerning diagno-ses, medication names, dosages, and fre-quency. Diabetes supplies, includingdiabetes medication, should accompanythe patient.

The sending facility must be mindfulof the transfer time in order to provide thepatient with medication and food ifneeded. The transfer summary or medicalrecord should be reviewed by a health

care provider upon arrival at the receivinginstitution.

Planning for patients’ discharge fromprisons should include instruction in thelong-term complications of diabetes, thenecessary lifestyle changes and examina-tions required to prevent these complica-tions, and, if possible, where patients mayobtain regular follow-up medical care. Aquarterly meeting to educate patientswith upcoming discharges about commu-nity resources can be valuable. Invitingcommunity agencies to speak at thesemeetings and/or provide writtenmaterialscan help strengthen the community linkfor patients discharging from correctionalfacilities.

Discharge planning for the patientswith diabetes should begin 1 monthbefore discharge. During this time, appli-cation for appropriate entitlementsshould be initiated. Any gaps in thepatient’s knowledge of diabetes careneed to be identified and addressed. It ishelpful if the patient is given a directory orlist of community resources and if anappointment for follow-up care with acommunity provider is made. A supply ofmedication adequate to last until the firstpostrelease medical appointment shouldbe provided to the patient upon release.The patient should be provided with awritten summary of his/her current heathcare issues, including medications anddoses, recent A1C values, etc.

Recommendationsc For all interinstitutional transfers,complete a medical transfer summaryto be transferred with the patient. (E)

c Diabetes supplies and medicationshould accompany the patient duringtransfer. (E)

c Begin discharge planning with ade-quate lead time to insure continuity of

care and facilitate entry into commu-nity diabetes care. (E)

SHARING OF MEDICALINFORMATION ANDRECORDSdPractical considerationsmay prohibit obtaining medical recordsfrom providers who treated the patientbefore arrest. Intake facilities should im-plement policies that 1) define the cir-cumstances under which prior medicalrecords are obtained (e.g., for patientswho have an extensive history of treat-ment for complications); 2) identify per-son(s) responsible for contacting the priorprovider; and 3) establish procedures fortracking requests.

Facilities that use outside medicalproviders should implement policiesand procedures for ensuring that keyinformation (e.g., test results, diagnoses,physicians’ orders, appointment dates) isreceived from the provider and incorpo-rated into the patient’s medical chart aftereach outside appointment. The proce-dure should include, at a minimum, ameans to highlight when key informationhas not been received and designation of aperson responsible for contacting theoutside provider for this information.

All medical charts should containCBG test results in a specified, readilyaccessible section and should be reviewedon a regular basis.

CHILDREN AND ADOLESCENTSWITH DIABETESdChildren andadolescents with diabetes present specialproblems in disease management, evenoutside the setting of a correctional in-stitution. Children and adolescents withdiabetes should have initial and follow-upcare with physicians who are experiencedin their care. Confinement increases thedifficulty in managing diabetes in chil-dren and adolescents, as it does in adultswith diabetes. Correctional authoritiesalso have different legal obligations forchildren and adolescents.

Nutrition and activityGrowing children and adolescents havegreater caloric/nutritional needs thanadults. The provision of an adequateamount of calories and nutrients foradolescents is critical to maintaininggood nutritional status. Physical activityshould be provided at the same time eachday. If increased physical activity occurs,additional CBG monitoring is necessaryand additional carbohydrate snacks maybe required.

Table 2dMajor components of diabetes self-management education

Survival skillsc hypo-/hyperglycemiac sick day managementc medicationc monitoringc foot care

Daily management issuesc disease processc nutritional managementc physical activityc medicationsc monitoringc acute complicationsc risk reductionc goal setting/problem solvingc psychosocial adjustmentc preconception care/pregnancy/gestationaldiabetes management



Medical management and follow-upChildren and adolescents who are incar-cerated for extended periods should havefollow-up visits at least every 3 monthswith individuals who are experienced inthe care of children and adolescents withdiabetes. Thyroid function tests and fast-ing lipid and microalbumin measure-ments should be performed according torecognized standards for children andadolescents (12) in order to monitor forautoimmune thyroid disease and compli-cations and comorbidities of diabetes.

Children and adolescents with diabe-tes exhibiting unusual behavior shouldhave their CBG checked at that time.Because children and adolescents arereported to have higher rates of nocturnalhypoglycemia (13), consideration shouldbe given regarding the use of episodicovernight blood glucose monitoring inthese patients. In particular, this shouldbe considered in children and adolescentswho have recently had their overnight in-sulin dose changed.

PREGNANCYdPregnancy in awoman with diabetes is by definition ahigh-risk pregnancy. Every effort shouldbe made to ensure that treatment of thepregnant woman with diabetes meetsaccepted standards (14,15). It should benoted that glycemic standards are morestringent, the details of dietary manage-ment are more complex and exacting, in-sulin is the only antidiabetic agentapproved for use in pregnancy, and anumber of medications used in the man-agement of diabetic comorbidities areknown to be teratogenic and must be dis-continued in the setting of pregnancy.

SUMMARY AND KEYPOINTSdPeople with diabetes shouldreceive care that meets national stand-ards. Being incarcerated does not changethese standards. Patients must have accessto medication and nutrition needed tomanage their disease. In patients who donot meet treatment targets, medical and

behavioral plans should be adjusted byhealth care professionals in collaborationwith the prison staff. It is critical forcorrectional institutions to identify par-ticularly high-risk patients in need ofmore intensive evaluation and therapy,including pregnant women, patients withadvanced complications, a history of re-peated severe hypoglycemia, or recurrentDKA.

A comprehensive, multidisciplinaryapproach to the care of people with di-abetes can be an effective mechanism toimprove overall health and delay or pre-vent the acute and chronic complicationsof this disease.

AcknowledgmentsdThe following membersof the American Diabetes Association/NationalCommission on Correctional Health CareJoint Working Group on Diabetes Guidelinesfor Correctional Institutions contributed tothe revision of this document: Daniel L.Lorber, MD, FACP, CDE (chair); R. ScottChavez, MPA, PA-C; Joanne Dorman, RN,CDE, CCHP-A; Lynda K. Fisher, MD;Stephanie Guerken, RD, CDE; Linda B. Haas,CDE, RN; Joan V. Hill, CDE, RD; David Ken-dall, MD; Michael Puisis, DO; Kathy Salo-mone, CDE, MSW, APRN; Ronald M.Shansky, MD, MPH; and Barbara Wakeen,RD, LD.

References1. National Commission on Correctional

Health Care: The Health Status of Soon-to-Be Released Inmates: A Report to Congress.Vol. 1. Chicago, NCCHC, 2002

2. Hornung CA, Greifinger RB, Gadre S: AProjection Model of the Prevalence of Se-lected Chronic Diseases in the Inmate Pop-ulation. Vol. 2. Chicago, NCCHC, 2002,p. 39–56

3. Puisis M: Challenges of improving qualityin the correctional setting. In ClinicalPractice in Correctional Medicine. St. Louis,MO, Mosby-Yearbook, 1998, p. 16–18

4. American Diabetes Association: Standardsof medical care in diabetesd2012 (Posi-tion Statement).Diabetes Care35 (Suppl. 1):S76–S80

5. American Diabetes Association: Screeningfor type 2 diabetes (Position Statement).Diabetes Care 27 (Suppl. 1):S11–S14,2004

6. Krauss RM, Eckel RH, Howard B, AppelLJ, Daniels SR, Deckelbaum RJ, ErdmanJW Jr, Kris-Etherton P, Goldberg IJ,Kotchen TA, Lichtenstein AH, Mitch WE,Mullis R, Robinson K, Wylie-Rosett J, StJeor S, Suttie J, Tribble DL, Bazzarre TL:American Heart Association DietaryGuidelines: revision 2000: a statement forhealthcare professionals from the Nutri-tion Committee of the American HeartAssociation. Stroke 31:2751–2766, 2000

7. American Diabetes Association: Nutritionrecommendations and interventions fordiabetes (Position Statement). DiabetesCare 31 (Suppl. 1):S61–S78, 2008

8. American Diabetes Association: Hyper-glycemic crisis in diabetes (PositionStatement). Diabetes Care 27 (Suppl. 1):S94–S102, 2004

9. American Diabetes Association: Continu-ous subcutaneous insulin infusion (Posi-tion Statement). Diabetes Care 27 (Suppl.1):S110, 2004

10. American Diabetes Association: Tests ofglycemia in diabetes (Position Statement).Diabetes Care 27 (Suppl. 1):S91–S93,2004

11. American Diabetes Association: Nationalstandards for diabetes self-managementeducation (Standards and Review Criteria).Diabetes Care 31 (Suppl. 1):S97–S104, 2008

12. International Society for Pediatric andAdolescent Diabetes: Consensus Guidelines2000: ISPAD Consensus Guidelines for theManagement of Type 1 Diabetes Mellitus inChildren and Adolescents. Zeist, Nether-lands, Medical Forum International, 2000,p. 116, 118

13. Kaufman FR, Austin J, Neinstein A, Jeng L,Halyorson M, Devoe DJ, PitukcheewanontP: Nocturnal hypoglycemia detected withthe continuous glucose monitoring systemin pediatric patients with type 1 diabetes.J Pediatr 141:625–630, 2002

14. American Diabetes Association: Gestationaldiabetes mellitus (Position Statement). Di-abetes Care 27 (Suppl. 1):S88–S90, 2004

15. Jovanovic L (Ed.): Medical Management ofPregnancy Complicated by Diabetes. 4th ed.Alexandria, VA, American Diabetes Asso-ciation, 2009


Diabetes and EmploymentAMERICAN DIABETES ASSOCIATION

A s of 2010, nearly 26 million Amer-icans have diabetes (1), most ofwhom are or wish to be participat-

ing members of the workforce. Diabetesusually has no impact on an individual’sability to do a particular job, and indeedan employer may not even know that agiven employee has diabetes. In 1984,the American Diabetes Associationadopted the following position on em-ployment:

Any person with diabetes, whether insulin[treated] or non–insulin [treated], should beeligible for any employment for which he/sheis otherwise qualified.

Questions are sometimes raised by em-ployers about the safety and effectivenessof individuals with diabetes in a given job.When such questions are legitimatelyraised, a person with diabetes shouldbe individually assessed to determinewhether or not that person can safelyand effectively perform the particularduties of the job in question. This docu-ment provides a general set of guidelinesfor evaluating individuals with diabetesfor employment, including how an as-sessment should be performed and whatchanges (accommodations) in the work-place may be needed for an individualwith diabetes.

I. EVALUATINGINDIVIDUALS WITHDIABETES FOREMPLOYMENTdIt was once com-mon practice to restrict individuals withdiabetes from certain jobs or classes ofemployment solely because of the diag-nosis of diabetes or the use of insulin,without regard to an individual’s abilitiesor circumstances. Such “blanket bans”are medically inappropriate and ignorethe many advancements in diabetes man-agement that range from the types of

medications used to the tools used toadminister them and to monitor bloodglucose levels.

Employment decisions should notbe based on generalizations or stereo-types regarding the effects of diabetes.The impact of diabetes and its manage-ment varies widely among individuals.Therefore, a proper assessment of in-dividual candidates for employment orcurrent employees must take this vari-ability into account.

In addition, federal and state lawsrequire employers to make decisionsthat are based on assessment of thecircumstances and capabilities of theindividual with diabetes for the particu-lar job in question (2,3). Application ofblanket policies to individuals with di-abetes results in people with diabetes be-ing denied employment for which theyare well qualified and fully capable ofperforming effectively and safely. Itshould be noted that, as a result ofamendments to the Americans with Dis-abilities Act, which became effective on1 January 2009, all persons with diabe-tes are considered to have a “disability”within the meaning of that law. This isbecause, among other reasons, diabetesconstitutes a substantial limitation onendocrine system functioningdthe Actwas amended to extend its coverage topersons with a substantial limitation in,among other things, a major bodilyfunction, such as the endocrine system.Therefore, persons with diabetes areprotected from discrimination in em-ployment and other areas. The amend-ments overturned a series of SupremeCourt decisions that had severely nar-rowed who was covered by the law andresulted in many people with diabetesand other chronic illnesses being deniedprotection from discrimination. Thissection provides an overview of the fac-tors relevant to a medically appropriate

individualized assessment of the candi-date or employee with diabetes.

Role of diabetes health careprofessionalsWhen questions arise about the medicalfitness of a person with diabetes for aparticular job, a health care professionalwith expertise in treating diabetes shouldperform an individualized assessment.The involvement of the diabetes healthcare professional should occur before anyadverse employment decision, such asfailure to hire or promote or termination.A health professional who is familiar withthe person with diabetes and who hasexpertise in treating diabetes is best ableto perform such an assessment. In somesituations and in complex cases, anendocrinologist or a physician who spe-cializes in treating diabetes or its compli-cations is the best qualified healthprofessional to assume this responsibility(4). The individual’s treating physician isgenerally the health care professionalwith the best knowledge of an individ-ual’s diabetes. Thus, even when the em-ployer utilizes its own physician toperform the evaluation, the opinions ofthe treating physician and other healthcare professionals with clinical expertisein diabetes should be sought out andcarefully considered. In situations wherethere is disagreement between the opin-ion of the employee’s treating physicianand that of the employer’s physician, theevaluation should be handed over to anindependent health care professionalwith significant clinical expertise indiabetes.

Individual assessmentA medical evaluation of an individualwith diabetes may occur only in limitedcircumstances (3). Employers may not in-quire about an individual’s health statusddirectly or indirectly and regardless ofthe type of jobdbefore making a job of-fer, but may require a medical examina-tion or make a medical inquiry once anoffer of employment has been extendedand before the individual begins the job.


Revised Fall 2009.DOI: 10.2337/dc12-s094© 2012 by the American Diabetes Association. Readers may use this article as long as the work is properly




The job offer may be conditioned on theresults of the medical inquiry or examina-tion. An employer may withdraw an offerfrom an applicant with diabetes only if itbecomes clear that he or she cannot do theessential functions of the job or wouldpose a direct threat (i.e., a significantrisk of substantial harm) to health orsafety and such threat could not be elim-inated with an accommodation (a work-place change that enables a worker with adisability to safely and effectively performjob duties). Another situation in whicha medical evaluation is permissible iswhen a problem potentially related tothe employee’s diabetes arises on the joband such problem could affect job perfor-mance and/or safety. In this situation, aphysician may be asked to evaluate theemployee’s fitness to remain on the joband/or his or her ability to safely performthe job.

Employers also may obtain medicalinformation about an employee when theemployee has requested an accomoda-tion and his or her disability or need foraccommodation is not obvious. An em-ployer should not rely on a medicalevaluation to deny an employment op-portunity to an individual with diabetesunless it is conducted by a health careprofessional with expertise in diabetes andbased on sufficient and appropriate med-ical data. The information sought andassessed must be properly limited to datarelevant to the individual’s diabetes andjob performance (3). The data needed willvary depending on the type of job and thereason for the evaluation, but an evalu-ation should never be made based onlyon one piece of data, such as a single bloodglucose result or A1C result. Since diabetesis a chronic disease in which health statusand management requirements naturallychange over time, it is inappropriatedand medically unnecessarydfor exam-iners to collect all past laboratory valuesor information regarding office visitswhether or not related to diabetes.Only medical information relevant toevaluating an individual’s current capac-ity for safe performance of the particularjob at issue should be collected. For ex-ample, in some circumstances a review ofan individual’s hypoglycemia historymaybe relevant to the evaluation and shouldbe collected.

Information about the individual’sdiabetes management (such as the currenttreatment regimen, medications, andblood glucose logs), job duties, andwork environment are all relevant factors

to be considered. Only health care profes-sionals tasked with such evaluationsshould have access to employee medicalinformation, and this information must bekept separate from personnel records (3).

Screening guidelinesA number of screening guidelines forevaluating individuals with diabetes invarious types of high risk jobs have beendeveloped in recent years. Examples in-clude the American College of Occupa-tional and Environmental Medicine’sNational Consensus Guideline for theMedical Evaluation of Law EnforcementOfficers, the National Fire ProtectionAssociation’s Standard on Comprehen-sive Occupational Medical Program forFire Departments, the U.S. Departmentof Transportation’s Federal Motor Car-rier Safety Administration’s DiabetesExemption Program, and the U.S. MarshallService and Federal Occupational HealthLaw Enforcement Program DiabetesProtocol.

Such guidelines and protocols can beuseful tools in making decisions aboutindividual candidates or employees ifthey are used in an objective way andbased on the latest scientific knowledgeabout diabetes and its management.These protocols should be regularly reeval-uated and updated to reflect changes indiabetes knowledge and evidence andshould be developed and reviewed byhealth care professionals with significantexperience in diabetes and its treatment.Individuals who do not meet the standardsset forth in such protocols should be giventhe opportunity to demonstrate excep-tional circumstances that would justifydeviating from the guidelines. Such guide-lines or protocols are not absolute criteriabut rather the framework for a thoroughindividualized assessment.

Recommendationsc People with diabetes should be in-dividually considered for employmentbased on the requirements of the spe-cific job and the individual’s medicalcondition, treatment regimen, andmedical history. (E)

c When questions arise about the medicalfitness of a person with diabetes for aparticular job, a health care professionalwith expertise in treating diabetesshould perform an individualized as-sessment; input from the treating phy-sician should always be included. (E)

c Employment evaluations should bebased on sufficient and appropriate

medical data and should never bemade based solely on one piece ofdata. (E)

c Screening guidelines and protocols canbe useful tools in making decisionsabout employment if they are used inan objective way and based on the latestscientific knowledge about diabetesand its management. (E)

II. EVALUATING THESAFETY RISK OFEMPLOYEES WITHDIABETESdEmployers who deny jobopportunities because they perceive allpeople with diabetes to be a safety riskdo so based on misconceptions, misin-formation, or a lack of current informationabout diabetes. The following guidelinesprovide information for evaluating an in-dividual with diabetes who works or seekstowork inwhatmaybe considered a safety-sensitive position.

Safety concernsThe first step in evaluating safety con-cerns is to determine whether the con-cerns are reasonable in light of the jobduties the individual must perform. Formost types of employment (such as jobsin an office, retail, or food service envi-ronment) there is no reason to believe thatthe individual’s diabetes will put employ-ees or the public at risk. In other types ofemployment (such as jobs where theindividual must carry a firearm or oper-ate dangerous machinery) the safety con-cern is whether the employee willbecome suddenly disoriented or inca-pacitated. Such episodes, which are usu-ally due to severely low blood glucose(hypoglycemia), occur only in peoplereceiving certain treatments such as in-sulin or secretagogues such as sulfonyl-ureas and even then occur infrequently.Workplace accommodations can bemade that are minimal yet effective inhelping the individual to manage his orher diabetes on the job and avoid severehypoglycemia.

HypoglycemiaHypoglycemia is defined as a bloodglucose level ,70 mg/dl (4,6). It is apotential side effect of some diabetestreatments, including insulin and sul-fonlyureas. It can usually be effectivelyself-treated by ingestion of glucose (carbo-hydrate) and is not often associated withloss of consciousness or a seizure. Severehypoglycemia, requiring the assistance ofanother person, is a medical emergency.


Position Statement

Symptoms of severe hypoglycemia mayinclude confusion or, rarely, seizure orloss of consciousness (6). Most individu-als with diabetes never experience an ep-isode of severe hypoglycemia becauseeither they are not on medication thatcauses it or they recognize the early warn-ing signs and can quickly self-treat theproblem by drinking or eating. Also,with self-monitoring of blood glucoselevels, most people with diabetes canmanage their condition in such a mannerthat there is minimal risk of incapacita-tion from hypoglycemia because mildlylow glucose levels can be easily detectedand treated (4,7).

A single episode of severe hypoglyce-mia should not per se disqualify an in-dividual from employment. Rather, anappropriate evaluation should be under-taken by a health care professional withexpertise in diabetes to determine thecause of the low blood glucose, the cir-cumstances of the episode, whether it wasan isolated incident, whether adjustmentto the insulin regimen may mitigate thisrisk, and the likelihood of such an episodehappening again. Some episodes of severehypoglycemia can be explained and cor-rected with the assistance of a diabeteshealth care professional.

However, recurrent episodes of se-vere hypoglycemia may indicate that anindividual may in fact not be able to safelyperform a job, particularly jobs or tasksinvolving significant risk of harm to em-ployees or the public, especially whenthese episodes cannot be explained. Theperson’s medical history and details ofany history of severe hypoglycemiashould be examined closely to determinewhether it is likely that such episodes willrecur on the job. In all cases, job dutiesshould be carefully examined to deter-mine whether there are ways to minimizethe risk of severe hypoglycemia (such asadjustment of the insulin regimen orproviding additional breaks to checkblood glucose levels).

HyperglycemiaIn contrast to hypoglycemia, high bloodglucose levels (hyperglycemia) can causelong-term complications over years or de-cades but does not normally lead to anyadverse effect on job performance. Thesymptoms of hyperglycemia generally de-velop over hours or days and do not occursuddenly. Therefore, hyperglycemia doesnot pose an immediate risk of sudden in-capacitation.While over years or decades,high blood glucose may cause long-term

complications to the nerves (neuropa-thy), eyes (retinopathy), kidneys (ne-phropathy), or heart, not all individualswith diabetes develop these long-termcomplications. Such complications be-come relevant in employment decisionsonly when they are established and in-terfere with the performance of the actualjob being considered. Evaluations shouldnot be based on speculation as to whatmight occur in the future. Job evaluationsshould take high blood glucose levels intoaccount only if they have already causedlong-term complications such as visualimpairment that interfere with perfor-mance of the specific job.

Aspects of a safety assessmentWhen an individual with diabetes isassessed for safety risk there are severalaspects that must be considered.Blood glucose test results. A singleblood glucose test result only gives infor-mation about an individual’s blood glucoselevel at one particular point in time. Be-cause blood glucose levels fluctuatethroughout the day (this is also true forpeople without diabetes), one test result isof no use in assessing the overall health of aperson with diabetes. The results of a seriesof self-monitored blood glucose measure-ments over a period of time, however, cangive valuable information about an indi-vidual’s diabetes health. Blood glucose re-cords should be assessed by a health careprofessional with expertise in diabetes (7).History of severe hypoglycemia. Of-ten, a key factor in assessing employmentsafety and risk is documentation of in-cidents of severe hypoglycemia. An in-dividual who has managed his or herdiabetes over an extended period of timewithout experiencing severe hypoglyce-mia is unlikely to experience this condi-tion in the future. Conversely, multipleincidents of severe hypoglycemia mayin some situations be disqualifying forhigh-risk occupations. However, thecircumstances of each incident shouldbe examined, as some incidents can beexplained due to changes in insulin dos-age, illness, or other factors and thus willbe unlikely to recur or have already beenaddressed by the individual throughchanges to his or her diabetes treatmentregimen or education.Hypoglycemia unawareness. Some in-dividuals over time lose the ability torecognize the early warning signs of hypo-glycemia. These individuals are at increasedrisk for a sudden episode of severe hypo-glycemia. Some of these individuals may

be able to lessen this risk with carefulchanges to their diabetes managementregimen (for example, more frequentblood glucose testing or frequent meals).Presence of diabetes-related complica-tions. Chronic complications that mayresult from long-term diabetes involve theblood vessels and nerves. These compli-cations may involve nerve (neuropathy),eye (retinopathy), kidney (nephropathy),and heart disease. In turn, these problemscan lead to amputation, blindness or othervision problems, including vision loss,kidney failure, stroke, or heart attack. Asthese complications could potentially affectjob performance and safety, such compli-cations should be evaluated by a specialistin the specific area related to the compli-cation. If complications are not present,their possible future development shouldnot be addressed, both because of lawsprohibiting such consideration and be-cause with medical monitoring and thera-pies, long-term complications can nowoften be avoided or delayed. Thus, manypeople with diabetes never develop any ofthese complications, and those that dogenerally develop them over a period ofyears.

Inappropriate assessmentsThe following tools and terms do notaccurately reflect the current state of di-abetes treatment and should be avoidedin an assessment of whether an individualwith diabetes is able to safely and effec-tively perform a particular job.Urine glucose tests. Urine glucose re-sults are no longer considered to be anappropriate and accurate methodologyfor assessing diabetes control (8). Beforethe mid-1970s, urine glucose tests werethe best available method of monitoringblood glucose levels. However, the urinetest is not a reliable or accurate indicatorof blood glucose levels and is a poor mea-sure of the individual’s current health sta-tus. Blood glucose monitoring is a moreaccurate and timely means to measureglycemic control. Urine glucose testsshould never be used to evaluate the em-ployability of a person with diabetes.A1C and estimated average glucose(eAG). Hemoglobin A1C (A1C) test re-sults reflect average glycemia over severalmonths and correlate with mean plasmaglucose levels (4). An eAG is directly re-lated to A1C and also provides an individ-ual with an estimate of average bloodglucose over a period of time, but it usesthe same values and units that are ob-served when using a glucose meter or


Diabetes and Employment

recording a fasting glucose value on a labreport (5). A1C/eAG values providehealth care providers with important in-formation about the effectiveness of anindividual’s treatment regimen (4) butare often misused in assessing whetheran individual can safely perform a job.Because they identify only averages andnot whether the person had severe ex-treme blood glucose readings, A1C/eAGresults are of no value in predicting short-term complications of diabetes and thushave no use in evaluating individuals inemployment situations.

The American Diabetes Associationrecommends that in most patients A1Clevels be kept below 7% (4), or eAG below154 mg/dl. This recommendation sets atarget in order to lessen the chances oflong-term complications of high bloodglucose levels but does not provide usefulinformation on whether the individual isat significant risk for hypoglycemia orsuboptimal job performance and is not ameasure of “compliance” with therapy.An A1C or eAG cut off score is not med-ically justified in employment evaluationsand should never be a determinative fac-tor in employment.“Uncontrolled” or “brittle” diabetes.Sometimes an individual’s diabetes is de-scribed as “uncontrolled,” “poorly con-trolled,” or “brittle.” These terms are notwell defined and are not relevant to jobevaluations. As such, giving an opinionon the level of “control” an individualhas over diabetes is not the same as assess-ing whether that individual is qualified toperform a particular job and can do sosafely. Such an individual assessment isthe only relevant evaluation.

Recommendationsc Evaluating the safety risk of employeeswith diabetes includes determiningwhether the concerns are reasonable inlight of the job duties the individualmust perform. (E)

c Most people with diabetes can managetheir condition in such a manner thatthere is no or minimal risk of incapaci-tation from hypoglycemia at work. Asingle episode of severe hypoglycemiashould not per se disqualify an individ-ual from employment, but an individualwith recurrent episodes of severe hypo-glycemia may be unable to safely per-form certain jobs, especially when thoseepisodes cannot be explained. (E)

c Hyperglycemia does not pose an imme-diate risk of sudden incapacitation onthe job, and long-term complications

are relevant in employment decisionsonly when they are established andinterfere with the performance of theactual job being considered. (E)

c Proper safety assessments should in-clude review of blood glucose test re-sults, history of severe hypoglycemia,presence of hypoglycemia unawareness,and presence of diabetes-related com-plications and should not include urineglucose or AIC/eAG tests or be basedon a general assessment of level of con-trol. (E)

III. ACCOMMODATINGEMPLOYEES WITHDIABETESdIndividuals with diabetesmay need certain changes or accommo-dations on the job in order to performtheir work responsibilities effectively andsafely. Federal and state laws require theprovision of “reasonable accommodations”to help an employee with diabetes to per-form the essential functions of the job (3).Additional lawsprovide for leave for an em-ployee to deal with his or hermedical needsor those of a family member (9). Althoughthere are some typical accommodationsthat many people with diabetes use, theneed for accommodations must be as-sessed on an individualized basis (2).

Accommodating daily diabetesmanagement needsMany of the accommodations that em-ployees with diabetes need on a day-to-day basis are those that allow them tomanage their diabetes in the workplace asthey would elsewhere. They are usuallysimple accommodations, can be providedwithout any cost to the employer, andshould cause little or no disruption in theworkplace. Most employers are requiredto provide accommodations unless thoseaccommodations would create an undueburden (3). Some accommodations thatmay be needed include the following.Testing blood glucose. Breaks may beneeded to allow an individual to testblood glucose levels when needed. Suchchecks only take minutes to complete.Some individuals use continuous glucosemonitors but will still need an opportu-nity to check blood glucose with a meter.Blood glucose can be checked whereverthe employee is without putting otheremployees at risk, and employers shouldnot limit where employees with diabetesare permitted to manage their diabetes.Some employees may prefer to have a pri-vate location for testing or other diabetes

care tasks that should be provided when-ever feasible.Administering insulin. Employees mayneed short breaks during the workday toadminister insulin when it is needed.Insulin can be safely administered wher-ever the employee happens to be. Theemployee may also need a place to storeinsulin and other supplies if work con-ditions (such as extreme temperatures)prevent the supplies from being carriedon the person (10).Food and drink. Employees may needaccess to food and/or beverages duringthe workday. This is particularly impor-tant in the event that the employee needsto quickly respond to low blood glucoselevels or maintain hydration if glucoselevels are high. Employees should bepermitted to consume food or beveragesas needed at their desk or work station(except in an extremely rare situation inwhich this would pose a hazard andcreate a safety issue, and if this is the case,an alternative site should be provided).Leave. Employees may need leave or aflexible work schedule to accommodatemedical appointments or other diabetescare needs. Occasionally, employees mayneed to miss work due to unanticipatedevents (severe hypoglycemic episode) orillness.Work schedules. Certain types of workschedules, such as rotating or split shifts,can make it especially difficult for someindividuals to manage diabetes effec-tively.

Accommodating complications ofdiabetesIn addition to accommodating the day-to-day management of diabetes in the work-place, for some individuals it is alsonecessary to seek modifications for long-term diabetes-related complications.Such people can remain productive em-ployees if appropriate accommodationsare implemented.

For example, an employee with di-abetic retinopathy or other vision impair-ments may benefit from using a big screencomputer or other visual aids, while anemployee with nerve pain may benefitfrom reduced walking distances or havingthe ability to sit down on the job. Indi-viduals with kidney problems may needto have flexibility to take time off work fordialysis treatment.

It is impossible to provide an exhaus-tive list of potential accommodations. Thekey message in accommodating an em-ployee with diabetes is to ensure that


Position Statement

accommodations are tailored to the in-dividual and effective in helping the in-dividual perform his or her job. Inputfrom health care professionals who spe-cialize in the particular complication, orfrom vocational rehabilitation specialistsor organizations, may help identify appro-priate accommodations.

Recommendationsc Individuals with diabetes may needaccommodations on the job in orderto perform their work responsibilitieseffectively and safely; these includeaccommodating daily diabetes needsand, when present, the complicationsof diabetes. All such accommodationsmust be tailored to the individual andeffective in helping the individual per-form his or her job. (E)

CONCLUSIONdIndividuals with di-abetes can and do serve as highly pro-ductive members of the workforce. Whilenot every individual with diabetes willbe qualified for, nor can perform, everyavailable job, reasonable accommoda-tions can readily be made that allow thevast majority of people with diabetes toeffectively perform the vast majority of

jobs. The therapies for, and effects of,diabetes vary greatly from person to per-son, so employers must consider eachperson’s capacities and needs on an in-dividual basis. People with diabetesshould always be evaluated individuallywith the assistance of experienced dia-betes health care professionals. The re-quirements of the specific job and theindividual’s ability to perform that job,with or without reasonable accommoda-tions, always need to be considered.

AcknowledgmentsdThe American DiabetesAssocation thanks the members of the volun-teer writing group for this updated statement:John E. Anderson, MD; Michael A. Greene, JD;JohnW. Griffin, Jr., JD; Daniel B. Kohrman, JD;Daniel Lorber,MD, FACP, CDE; Christopher D.Saudek, MD; Desmond Schatz, MD; and LindaSiminerio, RN, PhD, CDE.

References1. Centers for Disease Control and Pre-

vention: National Diabetes Fact Sheet:General Information and National Estimateson Diabetes and Prediabetes in the U.S., 2011.Atlanta, GA,U.S.Department ofHealth andHuman Services, Centers for Disease Con-trol and Prevention, 2011

2. Equal Employment Opportunity Com-mission, “Questions and Answers AboutDiabetes in the Workplace and theAmericans with Disabilities Act (ADA)”Oct. 29, 2003. Available from http://www.eeoc.gov/facts/diabetes.html. Accessed 26May 2008

3. Americans with Disabilities Act of 1990,42 U.S.C. x12101 et seq.

4. American Diabetes Association: Standardsof medical care in diabetesd2012 (Posi-tion Statement). Diabetes Care 2012;35(Suppl. 1): S76–S80

5. Nathan DM, Kuenen J, Borg R, Zheng H,Schoenfeld D, Heine R: Translating theA1C assay into estimated average glucosevalues. Diabetes Care 31: 1473–1478, 2008

6. American Diabetes Association: Definingand reporting hypoglycemia in diabetes,a report from the American Diabetes As-sociation Workgroup on Hypoglycemia.Diabetes Care 28: 1245–1249, 2005

7. American Diabetes Association: Self-monitoring of blood glucose (ConsensusStatement). Diabetes Care 17: 81–86, 1994

8. American Diabetes Association: Tests ofglycemia in diabetes (Position Statement).Diabetes Care 27 (Suppl. 1): S91–S93,2004

9. FamilyMedical LeaveAct of 1993, 29U.S.C.x2601 et seq.

10. American Diabetes Association: Insulin ad-ministration (Position Statement). DiabetesCare 27 (Suppl. 1): S106–S109, 2004


Diabetes and Employment

Third-Party Reimbursement forDiabetesCare, Self-Management Education,and SuppliesAMERICAN DIABETES ASSOCIATION

D iabetes is a chronic disease that af-fects nearly 26 million Americans(1) and is characterized by serious,

costly, and often fatal complications. Thetotal cost of diagnosed diabetes in the U.S.in 2007 was estimated to be $174 billion(2). To prevent or delay costly diabetescomplications and to enable people withdiabetes to lead healthy, productive lives,appropriate medical care based on currentstandards of practice, self-managementeducation, and medication and suppliesmust be available to everyone with diabe-tes. This paper is based on technical re-views titled “Diabetes Self-ManagementEducation” (3) and “National Standardsfor Diabetes Self-Management EducationPrograms” (4).

The goal of medical care for peoplewith diabetes is to optimize glycemic con-trol and minimize complications. The Di-abetes Control and Complications Trial(DCCT) demonstrated that treatment thatmaintains blood glucose levels near nor-mal in type 1 diabetes delays the onsetand reduces the progression of microvas-cular complications. The U.K. ProspectiveDiabetes Study (UKPDS) documentedthat optimal glycemic control can alsobenefit most individuals with type 2 dia-betes. To achieve optimal glucose control,the person with diabetes must be able toaccess health care providers who have ex-pertise in the field of diabetes. Treatmentplans must also include self-managementtraining and tools, regular and timely lab-oratory evaluations, medical nutritiontherapy, appropriately prescribed medi-cation(s), and regular self-monitoring ofblood glucose levels. The American Dia-betes Association position statement“Standards of Medical Care in Diabetes”

outlines appropriate medical care for peo-ple with diabetes (5).

An integral component of diabetescare is self-management education (in-patient and/or outpatient) delivered by aninterdisciplinary team. Self-managementtraining helps people with diabetes adjusttheir daily regimen to improve glycemiccontrol. Diabetes self-management edu-cation teaches individuals with diabetesto assess the interplay among medicalnutrition therapy, physical activity, emo-tional/physical stress, and medications,and then to respond appropriately andcontinually to those factors to achieve andmaintain optimal glucose control.

Today, self-management education isunderstood to be such a critical part ofdiabetes care that medical treatment ofdiabetes without systematic self-manage-ment education is regarded as inadequate.The “National Standards for Diabetes Self-Management Education” establish spe-cific criteria against which diabeteseducation programs can be measured,and a quality assurance program has beendeveloped and subsequently revised (6).

Treatments and therapies that im-prove glycemic control and reduce thecomplications of diabetes will also signif-icantly reduce health care costs (7,8). Nu-merous studies have demonstrated thatself-management education leads to re-ductions in the costs associated with alltypes of diabetes. Participants in self-management education programs havebeen found to have decreased lower-extremity amputation rates, reducedmedication costs, and fewer emergencyroom visits and hospitalizations.

To achieve optimal glycemic control,thus achieving long-term reduction in

health care costs, individuals with dia-betes must have access to the integralcomponents of diabetes care, such ashealth care visits, diabetes supplies, self-management education, and diabetes med-ications. As such, insurers must reimbursefor diabetes-related medical treatment aswell as for self-management educationprograms that have met accepted stand-ards, such as the American Diabetes Asso-ciation’s National Standards for DiabetesSelf-Management Education. Further-more, third-party payers must also reim-burse for medications and supplies relatedto the daily care of diabetes. These samestandards should also apply to organiza-tions that purchase health care benefits fortheir members or employees, as well asmanaged care organizations that provideservices to participants.

It is recognized that the use of formu-laries, prior authorization, competitivebidding, and related provisions (hereafterreferred to as “controls”) can manage pro-vider practices and costs to the potentialbenefit of payors and patients. Social Se-curity Act Title XIX, section 1927, statesthat excluded medications should nothave “a significant clinically meaningfultherapeutic advantage in terms of safety,effectiveness or clinical outcomes of suchtreatment of such population.”A variety oflaws, regulations, and executive ordersalso provide guidance on the use of suchcontrols to oversee the purchase and useof durable medical equipment (hereafterreferred to as “equipment”) and single-use medical supplies (hereafter referredto as “supplies”) associated with the man-agement of diabetes.

Certain principles should guide thecreation and enforcement of controls inorder to insure that they meet the com-prehensive medical needs of people livingwith diabetes. A wide array of medicationsand supplies are correlated with improvedglycemic outcomes and a reduction in therisk of diabetes-related complications. Be-cause no single diabetes treatment regimenis appropriate for all people with diabetes,providers and patients should have accessto a broad array ofmedications and suppliesto develop an effective treatment modality.


The recommendations in this paper are based on the evidence reviewed in the following publications: Diabetesself-management education (Technical Review). Diabetes Care 18:1204–1214, 1995; and National stand-ards for diabetes self-management education. Diabetes Care 33:S89–S96, 2010.

Approved 1995. Revised 2008DOI: 10.2337/dc12-s099© 2012 by the American Diabetes Association. Readers may use this article as long as the work is properly




However, the Association also recognizesthat there may be a number of medica-tions and/or supplies within any givenclass. As such, any controls should ensurethat all classes of antidiabetic agents withunique mechanisms of action are avail-able to facilitate achieving glycemic goalsto reduce the risk of complications. Sim-ilar issues operate in the management oflipid disorders, hypertension, and othercardiovascular risk factors, as well as forother diabetes complications. Further-more, any controls should ensure thatall classes of equipment and suppliesdesigned for use with such equipment areavailable to facilitate achieving glycemicgoals to reduce the risk of complications.It is important to note that medical ad-vances are rapidly changing the landscapeof diabetes medications and supplies. Toensure that patients with diabetes haveaccess to beneficial updates in treatmentmodalities, systems of controls must em-ploy efficient mechanisms through whichto introduce and approve new products.

Though it can seem appropriate forcontrols to restrict certain items in chronicdisease management, particularly with acomplex disorder such as diabetes, itshould be recognized that adherence is amajor barrier to achieving targets. Anycontrols should take into account thehuge mental and physical burden that in-tensive disease management exerts uponpatients with diabetes. Protections should

ensure that patients with diabetes canreadily comply with therapy in the widelyvariable circumstances encountered indaily life. These protections should guar-antee access to an acceptable range andall classes of antidiabetic medications,equipment, and supplies. Furthermore,fair and reasonable appeals processesshould ensure that diabetic patients andtheir medical care practitioners can obtainmedications, equipment, and suppliesthat are not contained within existentcontrols.

Diabetes management needs individ-ualization in order for patients to reachglycemic targets. Because there is diver-sity in the manifestations of the diseaseand in the impact of other medical con-ditions upon diabetes, it is common thatpractitioners will need to uniquely tailortreatment for their patients. To reachdiabetes treatment goals, practitionersshould have access to all classes of anti-diabetic medications, equipment, andsupplies without undue controls. With-out appropriate safeguards, these con-trols could constitute an obstruction ofeffective care.

The value of self-management edu-cation and provision of diabetes supplieshas been acknowledged by the passageof the Balanced Budget Act of 1997 (9)and by stated medical policy on both di-abetes education and medical nutritiontherapy.

References1. Centers for Disease Control and Preven-

tion. National estimates and general infor-mation on diabetes and prediabetes in the U.S.,2011. Atlanta,GA,U.S.Department of Healthand Human Services, Centers for DiseaseControl and Prevention, 2011

2. American Diabetes Association: Economiccosts of diabetes in the U.S. in 2007. Di-abetes Care 31: 596–615, 2008

3. Clement S: Diabetes self-management ed-ucation (Technical Review). Diabetes Care18: 1204–1214, 1995

4. Funnell MM, Haas LB: National standardsfor diabetes self-management educationprograms (Technical Review). DiabetesCare 18: 100–116, 1995

5. American Diabetes Association: Standardsof medical care in diabetesd2012 (PositionStatement). Diabetes Care 2012;35(Suppl.1):S11–S63

6. American Diabetes Association: Nationalstandards for diabetes self-management ed-ucation (Standards and Review Criteria).Diabetes Care 31 (Suppl. 1): S97–S104, 2008

7. Herman WH, Dasbach DJ, Songer TJ,Thompson DE, Crofford OB: Assessingthe impact of intensive insulin therapy onthe health care system.Diabetes Rev 2: 384–388, 1994

8. Wagner EH, Sandu N, Newton KM,McCullock DK, Ramsey SD, Grothaus LC:Effects of improved glycemic control onhealth care costs and utilization. JAMA 285:182–189, 2001

9. Balanced Budget Act of 1997. U.S. Govt.Printing Office, 1997, p. 115–116 (publ.no. 869-033-00034-1)


Third-party reimbursement

National Standards for DiabetesSelf-Management EducationMARTHA M. FUNNELL, MS, RN, CDE

1

TAMMY L. BROWN, MPH, RD, BC-ADM, CDE2

BELINDA P. CHILDS, ARNP, MN, CDE, BC-ADM3

LINDA B. HAAS, PHC, CDE, RN4

GWEN M. HOSEY, MS, ARNP, CDE5

BRIAN JENSEN, RPH6

MELINDA MARYNIUK, MED, RD, CDE7

MARK PEYROT, PHD8

JOHN D. PIETTE, PHD9,10

DIANE READER, RD, CDE11

LINDA M. SIMINERIO, PHD, RN, CDE12

KATIE WEINGER, EDD, RN7

MICHAEL A. WEISS, JD13

D iabetes self-management education(DSME) is a critical element of carefor all people with diabetes and is

necessary in order to improve patientoutcomes. The National Standards forDSME are designed to define quality di-abetes self-management education and toassist diabetes educators in a variety ofsettings to provide evidence-based edu-cation. Because of the dynamic nature ofhealth care and diabetes-related research,these Standards are reviewed and revisedapproximately every 5 years by key or-ganizations and federal agencies withinthe diabetes education community.

A Task Force was jointly convened bythe American Association of Diabetes Edu-cators and the American Diabetes Associa-tion in the summer of 2006. Additionalorganizations that were represented in-cluded the American Dietetic Association,the Veteran’s Health Administration, theCenters for Disease Control and Prevention,the Indian Health Service, and the AmericanPharmaceutical Association. Members ofthe Task Force included a person withdiabetes; several health services researchers/behaviorists, registerednurses, and registereddietitians; and a pharmacist.

The Task Force was charged withreviewing the current DSME standards for

their appropriateness, relevance, and sci-entific basis. The Standards were thenreviewed and revised based on the availableevidence and expert consensus. The com-mittee convened on 31 March 2006 and 9September 2006, and the Standards wereapproved 25 March 2007.

DEFINITION ANDOBJECTIVESdDiabetes self-manage-ment education (DSME) is the ongoingprocess of facilitating the knowledge,skill, and ability necessary for diabetesself-care. This process incorporates theneeds, goals, and life experiences of theperson with diabetes and is guided byevidence-based standards. The overallobjectives of DSMEare to support informeddecision-making, self-care behaviors,problem-solving and active collaborationwith the health care team and to improveclinical outcomes, health status, and qual-ity of life.

GUIDING PRINCIPLESdBeforethe review of the individual Standards,the Task Force identified overriding prin-ciples based on existing evidence thatwould be used to guide the review andrevision of the DSME Standards. Theseare:

1. Diabetes education is effective for im-proving clinical outcomes and qualityof life, at least in the short-term (1–7).

2. DSME has evolved from primarily di-dactic presentations to more theoreti-cally based empowerment models(3,8).

3. There is no one “best” education pro-gram or approach; however, programsincorporating behavioral and psycho-social strategies demonstrate improvedoutcomes (9–11). Additional studiesshow that culturally and age-appropriateprograms improve outcomes (12–16)and that group education is effective(4,6,7,17,18).

4. Ongoing support is critical to sustainprogress made by participants duringthe DSME program (3,13,19,20).

5. Behavioral goal-setting is an effectivestrategy to support self-managementbehaviors (21).

STANDARDS

StructureStandard 1. The DSME entity will havedocumentation of its organizational struc-ture, mission statement, and goals and willrecognize and support quality DSME as anintegral component of diabetes care.

Documentation of the DSME organi-zational structure, mission statement, andgoals can lead to efficient and effectiveprovision of services. In the businessliterature, case studies and case reportinvestigations on successful managementstrategies emphasize the importance ofclear goals and objectives, defined rela-tionships and roles, and managerial sup-port (22–25). While this concept isrelatively new in health care, businessand health policy experts and organiza-tions have begun to emphasize writtencommitments, policies, support, and theimportance of outcome variables in qual-ity improvement efforts (22,26–37). Thecontinuous quality improvement literaturealso stresses the importance of developingpolicies, procedures, and guidelines(22,26).

Documentation of the organizationalstructure, mission statement, and goalscan lead to efficient and effective pro-vision of DSME. Documentation of an orga-nizational structure that delineates channels


The previous version of the “National Standards for Diabetes Self-Management Education” was originallypublished in Diabetes Care 23:682–689, 2000. This version received final approval in March 2007.

From the 1Department of Medical Education, Diabetes Research and Training Center, University of Michigan,Ann Arbor, Michigan; 2Indian Health Service, Albuquerque, New Mexico; 3MidAmerica Diabetes Asso-ciates, Wichita, Kansas; the 4VA Puget Sound Health Care System, Seattle, Washington; the 5Division ofDiabetes Translation, National Center for Chronic Diseases Prevention and Health Promotion, Centers forDisease Control and Prevention, Atlanta, Georgia; 6Lakeshore Apothacare, Two Rivers, Wisconsin; the7Joslin Diabetes Center, Harvard Medical School, Boston, Massachusetts; 8Loyola College, Baltimore,Maryland; the 9VA Ann Arbor Health Care System, Ann Arbor, Michigan; the 10Department of InternalMedicine, Diabetes Research and Training Center, University of Michigan, Ann Arbor, Michigan; the11International Diabetes Center, Minneapolis, Minnesota; the 12Diabetes Institute, University of PittsburghMedical Center, Pittsburgh, Pennsylvania; and 13Patient Centered Solutions, Pittsburgh, Pennsylvania.

Corresponding author: Martha M. Funnell, [email protected]: 10.2337/dc12-s101© 2012 by the American Diabetes Association. Readers may use this article as long as the work is properly



S T A N D A R D S A N D R E V I E W C R I T E R I A

of communication and represents institu-tional commitment to the educational en-tity is critical for success (38–42).According to the Joint Commission on Ac-creditation of Health Care Organizations(JCAHO) (26), this type of documentationis equally important for small and largehealth care organizations. Health careand business experts overwhelminglyagree that documentation of the processof providing services is a critical factor inclear communication and provides a solidbasis fromwhich to deliver quality diabeteseducation (22,26,33,35–37). In 2005,JACHO published the Joint CommissionInternational Standards for Disease orCondition-Specific Care, which outlinesnational standards and performancemeasurements for diabetes and addressesdiabetes self-management education asone of seven critical elements (26).Standard 2. The DSME entity shall appointan advisory group to promote quality. Thisgroup shall include representatives from thehealth professions, people with diabetes, thecommunity, and other stakeholders.

Established and new systems (e.g.,committees, governing bodies, advisorygroups) provide a forum and a mecha-nism for activities that serve to guide andsustain the DSME entity (30,39–41).Broad participation of organization(s)and community stakeholders, includinghealth professionals, people with diabe-tes, consumers, and other communityinterest groups, at the earliest possiblemoment in the development, ongoingplanning, and outcomes evaluationprocess (22,26,33,35,36,41) can in-crease knowledge and skills about thelocal community and enhance collabo-rations and joint decision-making. Theresult is a DSME program that is patient-centered, more responsive to consumer-identified needs and the needs to thecommunity, more culturally relevant, andof greater personal interest to consumers(43–50).Standard 3. The DSME entity will deter-mine the diabetes educational needs of thetarget population(s) and identify resourcesnecessary to meet these needs.

Clarifying the target population anddetermining its self-management educa-tional needs serve to focus resources andmaximize health benefits (51–53). The as-sessment process should identify the ed-ucational needs of all individuals withdiabetes, not just those who frequentlyattend clinical appointments (51). DSMEis a critical component of diabetes treatment(2,54,55), yet the majority of individuals

with diabetes do not receive any formal di-abetes education (56,57). Thus, identifica-tion of access issues is an essential part ofthe assessment process (58). Demographicvariables, such as ethnic background, age,formal educational level, reading ability,and barriers to participation in education,must also be considered to maximize theeffectiveness of DSME for the target popu-lation (13–19,43–47,59–61).Standard 4. A coordinator will be desig-nated to oversee the planning, implementation,and evaluation of diabetes self-managementeducation. The coordinator will have aca-demic or experiential preparation in chronicdisease care and education and in programmanagement.

The role of the coordinator is essentialto ensure that quality diabetes educationis delivered through a coordinated andsystematic process. As new and creativemethods to deliver education are explored,the coordinator plays a pivotal role inensuring accountability and continuity ofthe educational process (23,60–62). Theindividual serving as the coordinator willbe most effective if there is familiaritywith the lifelong process of managing achronic disease (e.g., diabetes) and withprogram management.

ProcessStandard 5. DSME will be provided by oneor more instructors. The instructors will haverecent educational and experiential prepa-ration in education and diabetes manage-ment or will be a certified diabeteseducator. The instructor(s) will obtain reg-ular continuing education in the field of di-abetes management and education. At leastone of the instructors will be a registerednurse, dietitian, or pharmacist. A mecha-nism must be in place to ensure that the par-ticipant’s needs are met if those needs areoutside the instructors’ scope of practiceand expertise.

Diabetes education has traditionallybeen provided by nurses and dietitians.Nurses have been utilized most often asinstructors in the delivery of formal DSME(2,3,5,63–67). With the emergence ofmedical nutrition therapy (66–70), regis-tered dietitians became an integral part ofthe diabetes education team. In more re-cent years, the role of the diabetes educatorhas expanded to other disciplines, particu-larly pharmacists (73–79). Reviews com-paring the effectiveness of differentdisciplines for education report mixed re-sults (3,5,6). Generally, the literature fa-vors current practice that utilizes theregistered nurse, registered dietitian,

and the registered pharmacist as the keyprimary instructors for diabetes educationand members of the multidisciplinaryteam responsible for designing the curric-ulum and assisting in the delivery ofDSME (1–7,77). In addition to registerednurses, registered dietitians, andpharmacists, a number of studies reflectthe ever-changing and evolving healthcare environment and include otherhealth professionals (e.g., a physician,behaviorist, exercise physiologist, oph-thalmologist, optometrist, podiatrist)(48,80–84) and, more recently, lay healthand community workers (85–91) andpeers (92) to provide information, behav-ioral support, and linkswith the health caresystem as part of DSME.

Expert consensus supports the needfor specialized diabetes and educationaltraining beyond academic preparation forthe primary instructors on the diabetesteam (64,93–97). Certification as a diabe-tes educator by the National CertificationBoard for Diabetes Educators (NCBDE) isone way a health professional can demon-strate mastery of a specific body of knowl-edge, and this certification has become anaccepted credential in the diabetes com-munity (98). An additional credential thatindicates specialized training beyond basicpreparation is board certification in ad-vanced Diabetes Management (BC-ADM)offered by the American Nurses Creden-tialing Center (ANCC), which is availablefor master’s prepared nurses, dietitians,and pharmacists (48,84,99).

DSME has been shown to be mosteffective when delivered by a multidisci-plinary team with a comprehensive planof care (7,31,52,100–102). Within themultidisciplinary team, team memberswork interdependently, consult withone another, and have shared objectives(7,103,104). The team should have a col-lective combination of expertise in theclinical care of diabetes, medical nutritiontherapy, educational methodologies,teaching strategies, and the psychosocialand behavioral aspects of diabetes self-management. A referral mechanismshould be in place to ensure that the in-dividual with diabetes receives educationfrom those with appropriate training andcredentials. It is essential in this collabo-rative and integrated team approach thatindividuals with diabetes are viewed asleaders of their team and assume an activerole in designing their educational expe-rience (7,20,31,100–102,104).Standard 6. A written curriculum reflect-ing current evidence and practice guidelines,


Standards and Review Criteria

with criteria for evaluating outcomes, willserve as the framework for the DSME entity.Assessed needs of the individual with pre-diabetes and diabetes will determine whichof the content areas listed below are to beprovided:

c Describing the diabetes disease processand treatment options

c Incorporating nutritional managementinto lifestyle

c Incorporating physical activity into life-style

c Using medication(s) safely and for maxi-mum therapeutic effectiveness

c Monitoring blood glucose and other pa-rameters and interpreting and using theresults for self-management decisionmaking

c Preventing, detecting, and treating acutecomplications

c Preventing detecting, and treating chroniccomplications

c Developing personal strategies to ad-dress psychosocial issues and con-cerns

c Developing personal strategies to pro-mote health and behavior change

People with diabetes and their familiesand caregivers have a great deal to learn inorder to become effective self-managers oftheir diabetes. A core group of topics arecommonly part of the curriculum taughtin comprehensive programs that havedemonstrated successful outcomes(1,2,3,6,105–109). The curriculum, a co-ordinated set of courses and educationalexperiences, includes learning outcomesand effective teaching strategies (110–112). The curriculum is dynamic andneeds to reflect current evidence andpractice guidelines (112–117). Currenteducational research reflects the impor-tance of emphasizing practical, prob-lem-solving skills, collaborative care,psychosocial issues, behavior change,and strategies to sustain self-managementefforts (31,39,42,48,98,118–122).

The content areas delineated aboveprovide instructors with an outline fordeveloping this curriculum. It is impor-tant that the content be tailored to matcheach individual’s needs and adapted asnecessary for age, type of diabetes (includ-ing pre-diabetes and pregnancy), culturalinfluences, health literacy, and other co-morbidities (123,124). The content areasare designed to be applicable in all settingsand represent topics that can be developedin basic, intermediate, and advanced levels.Approaches to education that are interactive

and patient-centered have been shown tobe effective (83,119,121,122,125–127).

These content areas are presented inbehavioral terms and thereby exemplifythe importance of action-oriented, behav-ioral goals and objectives (13,21,55,121–123,128,129). Creative, patient-centeredexperience-based delivery methods areeffective for supporting informed decision-making and behavior change and go be-yond the acquisition of knowledge.Standard 7. An individual assessment andeducation plan will be developed collabora-tively by the participant and instructor(s) todirect the selection of appropriate educa-tional interventions and self-managementsupport strategies. This assessment and edu-cation plan and the intervention and out-comes will be documented in the educationrecord.

Multiple studies indicate the impor-tance of individualizing education basedon the assessment (1,56,68,131–135).The assessment includes informationabout the individual’s relevant medicalhistory, age, cultural influences, healthbeliefs and attitudes, diabetes knowledge,self-management skills and behaviors,readiness to learn, health literacy level,physical limitations, family support, andfinancial status (10–17,19,131,136–138). The majority of these studies sup-port the importance of attitudes andhealth beliefs in diabetes care outcomes(1,68,134,135,138,139).

In addition, functional health literacy(FHL) level can affect patients’ self-management, communication with clini-cians, and diabetes outcomes (140,141).Simple tools exist for measuring FHL aspart of an overall assessment process(142–144).

Many people with diabetes experi-ence problems due to medication costs,and asking patients about their abilityto afford treatment is important (144).Comorbid chronic illness (e.g., depres-sion and chronic pain) as well as moregeneral psychosocial problems can posesignificant barriers to diabetes self-management (104,146–151); consider-ing these issues in the assessment maylead to more effective planning (149–151).

Periodic reassessment determines at-tainment of the educational objectives orthe need for additional and creative in-terventions and future reassessment(7,97,100,152). A variety of assessmentmodalities, including telephone follow-up and other information technologies(e.g., Web-based, automated phone

calls), may augment face-to-face assess-ments (97,99).

While there is little direct evidence onthe impact of documentation on patientoutcomes, it is required to receive pay-ment for services. In addition, documen-tation of patient encounters guides theeducational process, provides evidence ofcommunication among instructionalstaff, may prevent duplication of services,and provides information on adherenceto guidelines (37,64,100,131,153). Pro-viding information to other members ofthe patient’s health care team throughdocumentation of educational objectivesand personal behavioral goals increasesthe likelihood that all of the memberswill address these issues with the patient(37,98,153).

Theuse of evidence-basedperformanceand outcome measures has been adoptedby organizations and initiatives such as theCenters forMedicare andMedicaid Services(CMS), theNational Committee for QualityAssurance (NCQA), the Diabetes QualityImprovement Project (DQIP), the HealthPlan Employer Data and Information Set(HEDIS), the Veterans AdministrationHealth System, and JCAHO (26,154).

Research suggests that the develop-ment of standardized procedures for doc-umentation, training health professionalsto document appropriately, and the use ofstructured standardized forms based oncurrent practice guidelines can improvedocumentation and may ultimately im-prove quality of care (100,153–155).Standard 8. A personalized follow-up planfor ongoing self management support will bedeveloped collaboratively by the participantand instructor(s). The patient’s outcomesand goals and the plan for ongoing self man-agement support will be communicated tothe referring provider.

While DSME is necessary, it is notsufficient for patients to sustain a lifetimeof diabetes self-care (55). Initial improve-ments in metabolic and other outcomesdiminish after;6 months (3). To sustainbehavior at the level of self-managementneeded to effectively manage diabetes,most patients need ongoing diabetesself-management support (DSMS).

DSMS is defined as activities to assistthe individual with diabetes to implementand sustain the ongoing behaviors neededtomanage their illness. The type of supportprovided can include behavioral, educa-tional, psychosocial, or clinical (13,121–123).

A variety of strategies are availablefor providing DSMS both within and



outside the DSME entity. Some patientsbenefit from working with a nurse casemanager (7,20,98,157). Case manage-ment for DSMS can include remindersabout needed follow-up care and tests,medication management, education, be-havioral goal-setting, and psychosocialsupport/ connection to community re-sources.

The effectiveness of providing DSMSthrough disease-management programs,trained peers and health communityworkers, community-based programs,use of technology, ongoing educationand support groups, and medical nutri-tion therapy has also been established(7,13,89–92,101,121–123,158–159).

While the primary responsibility fordiabetes education belongs to the DSMEentity, patients benefit by receiving re-inforcement of content and behavioralgoals from their entire health care team(100). Additionally, many patients re-ceive DSMS through their provider.Thus, communication is essential to en-sure that patients receive the supportthey need.

OutcomesStandard 9. The DSME entity will measureattainment of patient-defined goals and pa-tient outcomes at regular intervals using ap-propriate measurement techniques toevaluate the effectiveness of the educationalintervention.

In addition to program-defined goalsand objectives (e.g., learning goals, met-abolic, and other health outcomes), theDSME entity needs to assess each patient’spersonal self-management goals and his/her progress toward those personal goals.The AADE7 self-care behaviors provide auseful framework for assessment anddocumentation. Diabetes self-managementbehaviors include physical activity, healthyeating,medication taking,monitoringbloodglucose, diabetes self-care related problemsolving, reducing risks of acute and chroniccomplications, and psychosocial aspects ofliving with diabetes (112,160). Assess-ments of patient outcomes should occurat appropriate intervals. The interval de-pends on the outcome itself and the time-frame provided within the selected goals.For some areas, the indicators, measures,and timeframesmay be based on guidelinesfrom professional organizations or govern-ment agencies. In addition to assessingprogress toward personal behavioralgoals, a plan needs to be in place to com-municate personal goals and progress toother team members.

The AADE Outcome Standards for Di-abetes Education specify self-managementbehavior as the key outcome (112,160).Knowledge is an outcome to the degreethat it is actionable (i.e., knowledge thatcan be translated into self-management be-havior). In turn, effective self-management isone (but not the only) contributor to longer-term, higher-order outcomes such as clinicalstatus (e.g., control of glycemia, blood pres-sure, and cholesterol), health status (e.g.,avoidance of complications), and subjectivequality of life. Thus, patient self-manage-ment behaviors are at the core of the out-comes evaluation.Standard 10. The DSME entity will mea-sure the effectiveness of the education processand determine opportunities for improvementusing a written continuous quality improve-ment plan that describes and documents a sys-tematic review of the entities’ process andoutcome data.

Diabetes education must be respon-sive to advances in knowledge, treatmentstrategies, educational strategies, psycho-social interventions, and the changinghealth care environment. Continuousquality improvement (CQI) is an iterative,planned process (161) that leads to im-provement in the delivery of patient edu-cation (162). The CQI plan should definequality based on and consistent with theorganization’s mission, vision, and strate-gic plan and include identifying and pri-oritizing improvement opportunities(163). Once improvement projects areidentified and selected, the plan shouldincorporate timelines and importantmilestones including data collection,analysis, and presentation of results(163). Outcome measures indicate the re-sult of a process (i.e., whether changes areactually leading to improvement), whileprocess measures provide informationabout what caused those results (163–164). Process measures are often targetedto those processes that typically impactthe most important outcomes. Measuringboth process and outcomes helps to en-sure that change is successful withoutcausing additional problems in the system(164).

AcknowledgmentsdWork on this article wassupported in part by grant nos. NIH5P60DK20572 and 1 R18 0K062323 from theNational Institute of Diabetes and Digestiveand Kidney Diseases of the National Institutesof Health.The Task Force gratefully acknowledges the

assistance and support of Paulina Duker,MPH, APRN-BC, CDE, and Nathanial Clark,

MD, CDE, of the American Diabetes Associa-tion; Lori Porter, MBA, RD, CAE, of theAmerican Association of Diabetes Educators;and Karmeen Kulkarni, MS, RD, BC-ADM,Past President, Health Care and Education ofthe American Diabetes Association; MalindaPeeples, MS, RN, CDE, Past President of theAmerican Association of Diabetes Educators;and Carole’ Mensing, RN, MA, CDE, for theirinsights and helpful suggestions.We also gratefully acknowledge the work of

the previous Task Force for the NationalStandards for DSME: Carole’ Mensing, RN,MA, CDE; Jackie Boucher, MS, RD, LD, CDE;Marjorie Cypress, MS, C-ANP, CDE; KatieWeinger, EdD, RN; Kathryn Mulcahy, MSN,RN, CDE; Patricia Barta, RN, MPH, CDE;GwenHosey,MS, ARNP, CDE;WendyKopher,RN, C, CDE, HTP; Andrea Lasichak, MS, RD,CDE; Betty Lamb, RN, MSN; MavourneenMangan, RN, MS, ANP, C, CDE; Jan Norman,RD, CDE; Jon Tanja, BS, MS, RPH; Linda Yauk,MS, RD, LD, CDE; Kimberlydawn Wisdom,MD, MS; and Cynthia Adams, PhD

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Professional Practice Committee 2012Conflict of interest disclosures†

Member Employment Research grantOther research

support

Roger Austin, MS, RPH, CDE Henry Ford Health System, SterlingHeights, MI

None None

Susan Braithwaite, MD Endocrine Consultants & Care S.C.,Evanston, IL

None None

Martha Funnell, MSN, RN, CDE University of Michigan,Ann Arbor, MI

NIDDK, NIH, Peers for Progress None

Robert Gabbay, MD Pennsylvania State College of Medicine,Hershey, PA

NIDDK*, AHRQ* None

Richard Grant, MD, MPH Massachusetts General Hospital,Boston, MA

None None

Jane Kadohiro, DrPH, APRN, CDE The Queens Medical Center,Honolulu, HI

None None

James Lenhard, MD Christiana Care Health System Clinical pharmacology trialswith Macrogenics, sanofi-aventis,Lexicon, AstraZeneca*#

None

Daniel Lorber, MD Queens Diabetes and Endocrinology,Flushing, NY

Eli Lilly*, Johnson & Johnson*,Novo Nordisk*

None

Michelle Magee, MD Medstar Diabetes Institute,Washington, DC

sanofi-aventis*, Johnson & Johnson,Bayer, ESAI*, Boehringer Ingelheim*,Microsoft, GE*, ADA*

None

Sunder Mudaliar, MD VA San Diego Healthcare System,San Diego, CA

sanofi-aventis*#, Amylin*#,Daiichi-Sankyo*#, Astra-Zeneca*#

None

Patrick O’Connor, MD, MPH HealthPartners Research Foundation,Bloomington, MD

NHLBI/NIH*, NIDDK/NIH* Agency forHealthcare Research and Quality*,National Institute of MentalHealth/NIH*

None

R. Harsha Rao, MD University of Pittsburg, Pittsburg, PA None None

Andrew Rhinehart, MD, CDE Johnston Memorial Diabetes Center,Abingdon, VA

None None

Stuart Weinzimer, MD Yale University, New Haven, CT None None

Carol Wysham, MD (Chair) Rockwood Clinic, Spokane, WA None None

Gretchen Youssef, MS, RD, CDE Medstar Diabetes Institute,Washington, DC

None None

Judy Fradkin, MD (Ex officio) NIDDK, Bethesda, MD None NoneStephanie Dunbar, RD, MPH (Staff) ADA, Alexandria, VA None NoneSue Kirkman, MD (Staff) ADA, Alexandria, VA None None†Updated as of 20 October 2011. *$$10,000. #money goes to employer. xPatent application filed by VA Technology Transfer Program, DC01-#145823-v1-066072-0050, System andMethod for Automated Diabetes Control (Rao RH, Perreiah PL, Cunningham CA, Inventors). ADA, American Diabetes Association; AHRQ, Agencyfor Healthcare Research andQuality; CME, continuingmedical education; DSME, diabetes self-management education; ESAI, Endogenous StemCells Activators Inc.;NDEP, National Diabetes Education Program; NHLBI, National Heart Lung and Blood Institute; NIDDK, National Institute of Diabetes and Digestive and KidneyDiseases; NIH, National Institutes of Health; SHM, Society of Hospital Medicine.


MemberSpeakers’ bureau/

honoraria Ownership interest Consultant/advisory board Other

R.A. None None Amylin Pharmaceuticals, TakedaPharmaceuticals

None

S.B. None None None None

M.F. None None Eli Lilly, Halozyne Therapeutics,Bristol-Myers Squibb/AstraZenecaDiabetes, Hygeia Inc., BoehringerIngelheim, Johnson & Johnson,Animas/LifeScan, Intuity Medical,Bayer

NDEP Chair*

R.G. None None Roche None

R.G. None None Joslin Diabetes Center None

J.K. Johnson & JohnsonDiabetes Institute

None None None

J.L. AstraZeneca, Amylin,Merck, sanofi-aventis

None sanofi-aventis Expert witness forvariety of legal firms

D.L. Novo Nordisk* Biodel* Novo Nordisk*, Merck* Biodel (Board ofDirectors)*

M.M. sanofi-aventis*, NovoNordisk#

None sanofi-aventis*, SHM D.C. Department ofHealth* (CommunityEducation), Medscape(CME Program),Novo Nordisk*(Education Program)

S.M. American College of Physicians,Bristol-Myers Squibb/AstraZeneca, BoehringerIngelheim,

None Daiichi-Sankyo None

P.O. Park Nicollett Medical Center#,ADA Postgraduate Course#

Equity interest in SimCareHealth to market decisionsupport technology(company about tobe formed)

None Patent pending onsoftware for clinicaldecision supportrelated to diabetescare

R.R. None Co-inventor of GENIE. Nocommercial agreementsor collaborationsx

None None

A.R. Forest Laboratories*, Takeda,Abbott Laboratories, Eli Lilly,Novo Nordisk*, sanofi-aventis

None sanofi-aventis, Valeritas National StandardDSME UpdateWorkgroup

S.W. Eli Lilly None Animas/LifeScan, Becton-Dickinson,Medtronic, Novo Nordisk

None

C.W. Amylin Pharmaceuticals*, Eli Lilly*,Merck*, Novo Nordisk*,sanofi-aventis*, BoehringerIngelhiem

None Amylin Pharmaceuticals*,Boehringer Ingelheim, Eli Lilly*,Johnson & Johnson

None

G.Y. None None Novo Nordisk, Bayer Diagnostics None

J.F. None None None NoneS.D. None None None NoneS.K. None None None None


Professional Practice Committee

Systematic Reviews

A technical review is a balanced reviewand analysis of the literature on a scien-tific or medical topic related to diabetes.The technical review provides a scien-tific rationale for a position statement andundergoes critical peer review before sub-mission to the Professional Practice Com-mittee for approval. Effective January2010, technical reports were replacedwith systematic reviews, for which a pri-ori search and inclusion/exclusion criteriaare developed and published. Listed be-low are recent reviews.

Cost-Effectiveness of Diabetes Inter-ventionsLi R, Zhang P, Barker LE, ChowdhuryFM, Zhang X: Cost-effectiveness of inter-ventions to prevent and control diabetes

mellitus: a systematic review. DiabetesCare 33:1872–1894, 2010

ExerciseSigal RJ, Kenny GP, Wasserman DH,Castaneda-Sceppa C: Physical activity/exercise and type 2 diabetes. DiabetesCare 27:2518–2539, 2004

HospitalsClement S, Braithwaite SS, Magee MF,Ahmann A, Smith EP, Schafer RG, HirshIB: Management of diabetes and hyper-glycemia in hospitals. Diabetes Care 27:553–591, 2004

HypoglycemiaCryer PE, Davis SN, Shamoon H: Hypo-glycemia in diabetes. Diabetes Care 26:1902–1912, 2003

NeuropathyVinik AI,Maser RE,Mitchell BD, FreemanR: Diabetic autonomic neuropathy. Dia-betes Care 26:1553–1579, 2003

Boulton AJ,Malik RA, Arezzo JC, SosenkoJM: Diabetic somatic neuropathies. Dia-betes Care 27:1458–1486, 2004

RetinopathyFong DS, Aiello LP, Ferris FL III, Klein R:Diabetic retinopathy. Diabetes Care 27:2540–2553, 2004

Tests of GlycemiaGoldstein DE, Little RR, Lorenz RA,Malone JI, Nathan D, Peterson CM, SacksDB: Tests of glycemia in diabetes.DiabetesCare 27:1761–1773, 2004

e110 DIABETES CARE, VOLUME 35, SUPPLEMENT 1, JANUARY 2012 care.diabetesjournals.org

Consensus Reports

Effective January 2010, prior reports of the types listed below were renamed “consensus reports.”

EXPERT COMMITTEE REPORTSInternational Expert Committee Re-port on the Role of the A1C Assay inthe Diagnosis of DiabetesInternational Expert CommitteeDiabetes Care 32:1327–1334, 2009

Follow-Up Report on the Diagnosis ofDiabetes MellitusExpert Committee on the Diagnosis andClassification of DiabetesDiabetes Care 26:3160–3167, 2003

WORKGROUP REPORTSThe Charcot Foot in DiabetesLee C. Rogers, Robert G. Frykberg, DavidG. Armstrong, Andrew J.M. Boulton,Michael Edmonds, Georges Ha Van,Agnes Hartemann, Frances Game, WilliamJeffcoate,Alexandra Jirkovska, Edward Jude,Stephan Morbach, William B. Morrison,Michael Pinzur,Dario Pitocco, Lee Sanders,Dane K. Wukich, and Luigi UccioliDiabetes Care 34:2123–2129, 2011

Comprehensive Foot Examination andRisk Assessment: a Report of the TaskForce of the Foot Care Interest Groupof the American Diabetes Association,With Endorsement by the AmericanAssociation of Clinical Endocrinolo-gistsAndrew J.M. Boulton,DavidG.Armstrong,Stephen F. Albert, Robert G. Frykberg,Richard Hellman, M. Sue Kirkman,Lawrence A. Lavery, Joseph W. LeMaster,Joseph L. Mills, Sr., Michael J. Mueller,Peter Sheehan, and Dane K. WukichDiabetes Care 31:1679–1685, 2008

American Diabetes Association State-ment on Emergency and Disaster Pre-paredness: a Report of the DisasterResponse Task ForceDisaster Response Task ForceDiabetes Care 30:2395–2398, 2007

CONSENSUS REPORTSDiabetes and CancerEdward Giovannucci, David M. Harlan,Michael C. Archer, RichardM. Bergenstal,Susan M. Gapstur, Laurel A. Habel, Mi-chael Pollak, Judith G. Regensteiner, andDouglas Yee

Diabetes Care 33:1674–1685, 2010

Medical Management of Hyperglyce-mia in Type 2 Diabetes: A ConsensusAlgorithm for the Initiation and Ad-justment of Therapy: A ConsensusStatement of the American DiabetesAssociation and the European Associa-tion for the Study of DiabetesDavid M. Nathan, John B. Buse, Mayer B.Davidson, Ele Ferrannini, Rury R. Hol-man, Robert Sherwin, and Bernard Zin-man

Diabetes Care 32:193–203, 2009

AmericanAssociation of Clinical Endo-crinologists andAmericanDiabetes As-sociation Consensus Statement onInpatient Glycemic ControlEtie S. Moghissi, Mary T. Korytkowski,Monica DiNardo, Daniel Einhorn, Ri-chard Hellman, Irl B. Hirsch, Silvio E.Inzucchi, Faramarz Ismail-Beigi, M. SueKirkman, and Guillermo E. UmpierrezDiabetes Care 32:1119–1131, 2009

Hyperglycemic Crises in Adult Pa-tients With DiabetesAbbas E. Kitabchi, Guillermo E. Umpier-rez, John M. Miles, and Joseph N. FisherDiabetes Care 32:1335–1343, 2009

How Do We Define Cure of Diabetes?John B. Buse, Sonia Caprio, William T.Cefalu, Antonio Ceriello, Stefano DelPrato, Silvio E. Inzucchi, SueMcLaughlin,Gordon L. Phillips II, R. Paul Robertson,Francesco Rubino, Richard Kahn, and M.Sue Kirkman.Diabetes Care 32:2133–2135, 2009

Management ofHyperglycemia in Type2 Diabetes: A Consensus Algorithmfor the Initiation and Adjustment ofTherapy: Update Regarding Thiazo-lidinediones: a Consensus StatementFrom the American Diabetes Associa-tion and the European Association forthe Study of DiabetesDavid M. Nathan, John B. Buse, Mayer B.Davidson, Ele Ferrannini, Rury R. Holman,Robert Sherwin, and Bernard ZinmanDiabetes Care 31:173–175, 2008

Lipoprotein Management in PatientsWith Cardiometabolic Risk: Consen-sus Statement From the American Di-abetes Association and the AmericanCollege of Cardiology FoundationJohn D. Brunzell, Michael Davidson, CurtD. Furberg, Ronald B. Goldberg, BarbaraV. Howard, James H. Stein, and Joseph L.WitztumDiabetes Care 31:811–822, 2008

Managing Preexisting Diabetes forPregnancy: Summary of Evidence andConsensus Recommendations for CareJohn L. Kitzmiller, Jennifer M. Block,Florence M. Brown, Patrick M. Catalano,Deborah L. Conway, Donald R. Coustan,Erica P. Gunderson, William H. Herman,Lisa D. Hoffman, Maribeth Inturrisi, LoisB. Jovanovic, Siri I. Kjos, Robert H. Knopp,Martin N. Montoro, Edward S. Ogata,Pathmaja Paramsothy, Diane M. Reader,Barak M. Rosenn, Alyce M. Thomas, andM. Sue KirkmanDiabetes Care 31:1060–1079, 2008

Influence of Race, Ethnicity, andCultureon Childhood Obesity: Implications forPrevention and Treatment: A ConsensusStatement of Shaping America’s Healthand the Obesity SocietySonia Caprio, Stephen R. Daniels, AdamDrewnowski, Francine R. Kaufman, Law-rence A. Palinkas, Arlan L. Rosenbloom,and Jeffrey B. SchwimmerDiabetes Care 31:2211–2221, 2008

Screening for Coronary Artery Diseasein Patients With DiabetesJeroen J. Bax, Lawrence H. Young, RobertL. Frye, Robert O. Bonow, Helmut O.Steinberg, and Eugene J. BarrettDiabetes Care 30:2729–2736, 2007

Consensus Statement on the World-wide Standardization of the Hemoglo-bin A1C Measurement: the AmericanDiabetes Association, European Asso-ciation for the Study of Diabetes,International Federation of ClinicalChemistry and Laboratory Medicine,and the International Diabetes Federa-tion

care.diabetesjournals.org DIABETES CARE, VOLUME 35, SUPPLEMENT 1 JANUARY 2012 e111

Consensus CommitteeDiabetes Care 30:2399–2400, 2007

Use of Insulin Pump Therapy in the Pe-diatric Age-Group: Consensus State-ment From the European Society forPaediatric Endocrinology, the LawsonWilkins Pediatric Endocrine Society,and the International Society for Pedi-atric and Adolescent Diabetes, En-dorsed by the American DiabetesAssociation and the European Associa-tion for the Study of DiabetesMoshe Phillip, Tadej Battelino, HenryRodriguez, Thomas Danne, FrancineKaufman for the Consensus forum par-ticipantsDiabetes Care 30:1653–1662, 2007

Waist Circumference and Cardiometa-bolic Risk: a Consensus StatementFrom Shaping America’s Health: Asso-ciation for Weight Management andObesity Prevention; NAASO, The Obe-sity Society; the American Society forNutrition; and the American DiabetesAssociationSamuel Klein, David B. Allison, Steven B.Heymsfield, David E. Kelley, Rudolph L.Leibel, Cathy Nonas, and Richard KahnDiabetes Care 30:1647–1652, 2007

Computer Modeling of Diabetes andIts Complications: a Report on theFourth Mount Hood Challenge MeetingThe Mount Hood 4 Modeling GroupDiabetes Care 30:1638–1646, 2007

Impaired Fasting Glucose and Im-paired Glucose Tolerance: Implica-tions for CareDavid M. Nathan, Mayer B. Davidson,Ralph A. DeFronzo, Robert J. Heine,Robert R. Henry, Richard Pratley, andBernard ZinmanDiabetes Care 30:753–759, 2007

Diabetic Ketoacidosis in Infants, Chil-dren, and Adolescents: A ConsensusStatement From the American Diabe-tes AssociationJoseph Wolfsdorf, Nicole Glaser, andMark A. SperlingDiabetes Care 29:1150–1159, 2006

e112 DIABETES CARE, VOLUME 35, SUPPLEMENT 1 JANUARY 2012 care.diabetesjournals.org

Position Statements

A position statement is an official pointof view or belief of the ADA. Positionstatements are issued on scientific ormedical issues related to diabetes. Theymay be authored or unauthored and arepublished in ADA journals and otherscientific/medical publications as appro-priate. Position statements must be re-viewed and approved by the ProfessionalPractice Committee and, subsequently,by the Executive Committee of the Boardof Directors. ADA position statements aretypically based on a technical review orother review of published literature. Theyare reviewed on an annual basis and upda-ted as needed. In addition to those pub-lished in this supplement, listed below arerecent position statements.

Laboratory Analysis in the Diagnosisand Management of Diabetes MellitusDavid B. Sacks, Mark Arnold, George L.Bakris, David E. Bruns, Andrea RitaHorvath,M. Sue Kirkman, Ake Lernmark,Boyd E. Metzger, and David M. NathanDiabetes Care 34:1419–1423, 2011

Recommendations for TransitionFrom Pediatric to Adult DiabetesCare Systems:A position statement of the AmericanDiabetes Association, with representationby the American College of OsteopathicFamily Physicians, the American Acad-emy of Pediatrics, the American Associ-ation of Clinical Endocrinologists, theAmerican Osteopathic Association, theCenters for Disease Control and Prevention,Children with Diabetes, The Endocrine So-ciety, the International Society for Pediatricand Adolescent Diabetes, Juvenile DiabetesResearch FoundationInternational, theNational Diabetes Education Program, andthe Pediatric Endocrine Society (formerlyLawsonWilkins Pediatric Endocrine Society)Diabetes Care 34:2477–2485, 2011

Aspirin for Primary Prevention ofCardiovascular Events in PeopleWith Diabetes: A Position Statementof the American Diabetes

Association, a Scientific Statementof the American Heart Association,and an Expert Consensus Documentof the American College ofCardiology FoundationMichael Pignone, Mark J. Alberts, John A.Colwell, Mary Cushman, Silvio E. Inzuc-chi, Debabrata Mukherjee, Robert S.Rosenson, Craig D. Williams, Peter W.Wilson, and M. Sue KirkmanDiabetes Care 33:1395–1402, 2010

Exercise and Type 2 Diabetes: TheAmerican College of Sports Medicineand the American DiabetesAssociation: Joint PositionStatementSheri R. Colberg, Ronald J. Sigal, Bo Fern-hall, Judith G. Regensteiner, Bryan J.Blissmer, Richard R. Rubin, Lisa Chasan-Taber, Ann L. Albright, and Barry BraunDiabetes Care 33:e147–e167, 2010

Clinical Care Guidelines for CysticFibrosis–Related Diabetes: APosition Statement of the AmericanDiabetes Association and a ClinicalPractice Guideline of the CysticFibrosis Foundation, Endorsed bythe Pediatric Endocrine SocietyAntoinette Moran, Carol Brunzell, RichardC. Cohen, Marcia Katz, Bruce C. Marshall,Gary Onady, Karen A. Robinson, KathrynA. Sabadosa, Arlene Stecenko, and BonnieSlovis, the CFRD Guidelines CommitteeDiabetes Care 33:2697–2708, 2010

Intensive Glycemic Control and thePrevention of Cardiovascular Events:Implications of the ACCORD,ADVANCE, and VA Diabetes Trials:A Position Statement of theAmerican Diabetes Association anda Scientific Statement of theAmerican College of CardiologyFoundation and the American HeartAssociationJay S. Skyler, Richard Bergenstal, RobertO. Bonow, John Buse, Prakash Deedwania,Edwin A.M. Gale, Barbara V. Howard,M. Sue Kirkman, Mikhail Kosiborod, PeterReaven, and Robert S. Sherwin

Diabetes Care 32:187–192, 2009

Nutrition Recommendations andInterventions for Diabetes: A PositionStatement of the American DiabetesAssociationAmerican Diabetes AssociationDiabetes Care 31 (Suppl. 1):S61–S78, 2008

Generic Drugs: A Position Statementof the American DiabetesAssociationAmerican Diabetes AssociationDiabetes Care 30:173, 2007

Pancreas and Islet Transplantationin Type 1 Diabetes: A Positionof the AmericanDiabetes AssociationAmerican Diabetes AssociationDiabetes Care 29:935, 2006

The Metabolic Syndrome: Time for aCritical Appraisal: Joint StatementFrom the American DiabetesAssociation and the EuropeanAssociation for the Study ofDiabetesRichard Kahn, John Buse, Ele Ferrannini,and Michael SternDiabetes Care 28:2289, 2005

Diabetic Neuropathies: A Statementby the American DiabetesAssociationAndrew J.M. Boulton, Arthur I. Vinik, Jo-seph C. Arezzo, Vera Bril, Eva L. Feldman,Roy Freeman, Rayaz A. Malik, RaeleneE. Maser, Jay M. Sosenko, and Dan ZieglerDiabetes Care 28:956, 2005

Care of Children and AdolescentsWith Type 1 Diabetes: A Statementof the American DiabetesAssociationJanet Silverstein, Georgeanna Klingen-smith, Kenneth Copeland, Leslie Plot-nick, Francine Kaufman, Lori Laffel, LarryDeeb, Margaret Grey, Barbara Anderson,Lea Ann Holzmeister, and NathanielClarkDiabetes Care 28:186, 2005

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