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40 ENDOCRINE PRACTICE Vol. 8 (Suppl. 1) January/February 2002 The American Association of Clinical Endocrinologists Medical Guidelines for the Management of Diabetes Mellitus: The AACE System of Intensive Diabetes Self-Management—2002 Update Developed by the American Association of Clinical Endocrinologists and the American College of Endocrinology—2002

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Page 1: The American Association of Clinical Endocrinologists Medical ...diabetesindia.com/diabetes/diabetes_2002.pdf · Management of Diabetes Mellitus. A key component of the AACE system

40 ENDOCRINE PRACTICE Vol. 8 (Suppl. 1) January/February 2002

The American Association of Clinical Endocrinologists

Medical Guidelines for the Management of Diabetes Mellitus:

The AACE System of

Intensive Diabetes Self-Management—2002 Update

Developed by theAmerican Association of Clinical Endocrinologists

and the American College of Endocrinology—2002

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In 1994, the American Association of Clinical Endo-crinologists (AACE) developed a System of IntensiveDiabetes Self-Management. This system remains the cen-terpiece of the AACE Medical Guidelines for theManagement of Diabetes Mellitus. A key component ofthe AACE system of care is a patient-physician contract,which maintains the preeminence of the patient-physicianrelationship and the importance of the patient’s participa-tion in personal care. As stated therein, the duties of thephysician and the diabetes management team are to teachand to help direct the patient’s own self-management.

The System of Intensive Diabetes Self-Managementincludes the concepts of care, the responsibilities of thepatient and the physician, and the appropriate intervals offollow-up assessment. Also included are the timing ofrequired laboratory testing, determined by evidence-basedand consensus clinical experience. As indicated in theoriginal publication of the guidelines, the intensive self-management system applies to patients with type 1 andtype 2 diabetes.

AACE brought these concepts directly to the publicwith two highly successful patient initiatives. These dia-betes initiatives were called “Patients First” and “PatientsFirst 1998.” The names of these initiatives emphasize thatthe treatment of the patient should be the first priority forthe patient, the physician, and all those providing health-care coverage. Access to appropriate care and durablemedical equipment should not be restricted. AACEemphasizes that the patient should demand access toappropriate care.

In addition, the patient, with a focus on self-manage-ment, must become a “Professor of Diabetes.” The physi-cian and the diabetes management team are responsible forhelping the patient achieve this expertise, and the clinicalendocrinologist is the physician best trained to make the

initial diagnosis and to recommend optimal treatment ofdiabetes.

During the past 5 years, many published studies haveconfirmed the importance of intensive diabetes self-man-agement, not only for type 1 but also for type 2 diabetes.There is now no doubt that control of diabetes is of utmostimportance. Furthermore, many new pharmacologicagents have been developed, some with unique mecha-nisms of action. The use of combinations of older and newpharmacologic agents enables the patient to achieve near-normalization of blood glucose levels.

Evidence continues to accumulate in support of theimportance of intensive diabetes self-management earlyduring the course of the disease as well as intensive con-trol of comorbid states, such as hypertension, dyslipi-demia, and obesity. The early control of comorbid statesdecreases the occurrence of complications of diabetes.Moreover, comorbid states can be precipitated orworsened by the occurrence of diabetes.

The 2000 revision of the AACE medical practiceguidelines focuses on the system of care provided in theoriginal guidelines but adds new evidence for manage-ment and treatment of type 1 and type 2 diabetes mellitus.The AACE System of Intensive Diabetes Self-Manage-ment remains intact. In this revision, we have emphasizedtype 2 diabetes because it is our conviction that type 2diabetes is an underrecognized but very serious diseasethat must be treated as aggressively as type 1 diabetesmellitus.

As chairman, I wish to thank the Diabetes MedicalGuidelines Task Force, Drs. Richard Hellman, RichardDickey, Paul Jellinger, John Janick, Helena Rodbard,Rhoda Cobin, David Bell, Om Ganda, Eugene Davidson,and John Seibel, for their valuable contributions to theserevised, expanded guidelines.

INTRODUCTION

Stanley Feld, MD, FACP, MACEChairman, Diabetes Medical Guidelines Task Force

AACE Diabetes Guidelines

ENDOCRINE PRACTICE Vol. 8 (Suppl. 1) January/February 2002 41

2002 UPDATE

The American College of Endocrinology (ACE) held a Diabetes Mellitus Consensus Conference, August20-21, 2001. The outcome of this ground breaking conference included new guidelines for HbA1c levels.Pre and postprandial targets, and a universal term for hemoglobin A1c. These guidelines have been revisedto reflect these outcomes. Also included in the 2002 version are changes in treatment that have occurredsince the publication of the 2000 version.

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42 AACE Diabetes Guidelines, Endocr Pract. 2002;8(Suppl 1)

Diabetes Medical Guidelines Task Force

Chairman

Stanley Feld, MD, MACE

Committee Members

Richard Hellman, MD, FACERichard A. Dickey, MD, FACP, FACE

Paul S. Jellinger, MD, FACEJohn J. Janick, MD, FACE

Helena W. Rodbard, MD, FACERhoda H. Cobin, MD, FACEDavid S. H. Bell, MB, FACE

Om Ganda, MD, FACEEugene T. Davidson, MD, MACE

John A. Seibel, MD, FACE

Reviewers

Robert J. Anderson, MD, FACEDonald A. Bergman, MD, FACE

H. Jack Baskin, MD, FACEBruce F. Bower, MD, FACE

Pauline Camacho, MDSamuel E. Crockett, MD, FACE

Daniel Einhorn, MD, FACEJeffrey R. Garber, MD, FACEHossein Gharib, MD, FACE

Carlos R. Hamilton, Jr., MD, FACEStephen F. Hodgson, MD, FACE

John S. Kukora, MD, FACEBill Law, Jr., MD, FACE

Claresa S. Levetan, MD, FACEPhilip Levy, MD, FACE

Pasquale J. Palumbo, MD, MACESteven M. Petak, MD, FACE

Krishna M. Pinnamanenni, MD, FACEHerbert I. Rettinger, MD, FACE

Harvey A. Rubenstein, MD, FACEPaul H. Saenger, MD, FACE

John B. Tourtelot, MD, LCDR, USNDavid A. Westbrock, MD, FACE

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MISSION STATEMENT

The results of the Diabetes Control and Complica-tions Trial (DCCT), announced in June 1993, confirmedthat the near-normalization of blood glucose levels inpatients with type 1 diabetes can significantly delay theonset and slow the progression of complications associat-ed with this disease (1). Near-normalization of blood glu-cose can be achieved by intensive control of diabetes (1).It has been established that the complications of diabetesare related to abnormalities in blood glucose (1). Manyendocrinologists contended that intensive control couldalso reduce the complications associated with type 2 dia-betes (2). At that time, AACE agreed that a system ofintensive control of diabetes mellitus would likelydecrease the rate of complications, improve the patient’squality of life, and decrease the total cost of care associat-ed with both type 1 and type 2 diabetes. Studies since thattime, including the United Kingdom Prospective DiabetesStudy (UKPDS) of 1998, have confirmed AACE’s notionthat the goal in type 2 diabetes must also be normalizationor near-normalization of the blood glucose level in orderto decrease associated complications (3-5).

A systematic multidisciplinary approach has beendeveloped to help clinical endocrinologists and otherphysicians provide intensive therapy for patients with dia-betes mellitus in an effort to achieve normal or near-nor-mal blood glucose levels. The primary requirements forthe successful implementation of this system of care areactive patient participation, a committed health-care team,and adherence to the schedule of recommended interac-tions between the patient and the health-care team.

The health-care team should be managed by a clinicalendocrinologist; ideally, the team should include a dia-betes-trained nurse, a dietitian skilled in diabetes educa-tion, and, as needed, a pharmacist, psychologist, and exer-cise physiologist. The team should be led by a clinicalendocrinologist or other physician who has expertise andexperience in overseeing and directing this integratedsystem of care. Of course, notable improvement in patientcare will be achieved when physicians of all specialties aremore aware of the relationship between blood glucosecontrol and diabetes-associated complications and arefamiliar with the steps for implementing a program ofintensive diabetes treatment. These guidelines, which areintended to assist in those efforts, now include the scien-tific evidence of recent years to support the AACE Systemof Intensive Diabetes Self-Management.

SECTION 1: INTENSIVE THERAPY IN TYPE 1AND TYPE 2 DIABETES

Mechanisms and GoalsCurrent strategies for optimal care of patients with

diabetes mellitus include vigorous and persistent efforts toachieve physiologic control of blood glucose and otheroften associated conditions including hypertension, dys-lipidemia, and excess weight. Abundant evidence is now

available that long-term maintenance of near-normalblood glucose levels is protective of patients with diabetesand substantially reduces complications and mortality inboth type 1 and type 2 diabetes (1,3-6). The term “inten-sive therapy” denotes a comprehensive program of dia-betes care that includes, as two of its components, frequentself-monitoring of blood glucose levels and more complexand sophisticated regimens for maintaining near-normo-glycemia—which, in the case of insulin treatment, ofteninvolves multiple insulin injections daily or subcutaneousinsulin infusion therapy (insulin pump therapy).

The DCCT (1) showed that, for patients with type 1diabetes, intensive insulin therapy including three or moreinsulin injections daily or use of an insulin pump was opti-mal management. This therapy also can be optimal formany patients with type 2 diabetes who may have insulindeficiency and therefore require insulin supplementation.Often included in this group are older patients, nonobesepatients, and patients with diabetes of long duration.

With the recent development of five major classes oforally administered antidiabetic agents, modern patterns ofintensive therapy in type 2 diabetes are now widelydiverse. In addition to medical nutrition therapy, the clini-cian often uses a wide variety of therapeutic regimens atdifferent times in the care of the patient with type 2 dia-betes. The decision for use of a specific treatment optionshould be in the hands of the leader of the diabetes careteam, the clinical endocrinologist, who should establishthe targets and choose the therapeutic agents for control ofblood glucose.

For each patient, therapy should be individualized tomaximize the likelihood of attaining and maintaining theappropriate goal and reducing the frequency of side effectsor adverse reactions. To date, several studies have found asignificant advantage associated with a decrease in glyco-sylated hemoglobin levels to 7.0% (normal, 3.8 to 6%), orlower if possible (1,3-6). Both preprandial and postprandi-al blood glucose targets are useful. The ACE DiabetesMellitus Consensus Conference in August 2001 estab-lished the following goals: HbA1c level of 6.5% or less;preprandial glucose of 110 mg/dL or less; and the postprandial glucose of 140 mg/dL or less.(6a)

Clearly, the method used to attain normoglycemia isless important than the fact that the goal is achieved. Thethreat of hypoglycemia seems to be much less serious intype 2 than in type 1 diabetes (3,4) and can often be mini-mized with more frequent blood glucose monitoring (6),more comprehensive educational intervention, and carefuladjustment of medication.

Emerging evidence indicates that intensive therapyand careful control of blood glucose levels are particular-ly important in achieving better diabetes-related outcomesin the setting of acute conditions (7,8). Data from theDIGAMI (Diabetes Mellitus and Insulin-Glucose Infusionin Acute Myocardial Infarction) Study (7) indicate thevalue of intensive insulin therapy during and after acutemyocardial infarction in patients with diabetes. Otherstudies have also shown the importance of maintaining

AACE Diabetes Guidelines, Endocr Pract. 2002;8(Suppl 1) 43

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normoglycemia during severe infections, cerebralischemia, or perioperative periods. Therefore, the clinicalendocrinologist serves an important role not only in theday-to-day care of the patient with diabetes but also in theacute-care setting.

Although the benefit of a more comprehensive andintensive approach for diabetes care is evident at any pointin the course of patient care (6), it is particularly importantearly during the course of the disease (1). The greatestbenefits have been noted in patients with less advanceddisease (1,5,6). Thus, prompt initial care and early referralto a clinical endocrinologist for preventive care in bothtype 1 and type 2 diabetes are not only logical and appro-priate but key to achieving the best clinical outcomepossible.

Diabetes Management TeamThe value of diabetes management teams is also

becoming clearer. The concept of active involvement ofthe patient in a self-management program is important;excellent results have been achieved when the patientactively participates as a member of the diabetes careteam. Adherence to complex regimens of care is consider-ably enhanced by this method. Of note, however, thepatient’s personal goals, particularly at the outset, may dif-fer substantially from the physician’s treatment goals.Nevertheless, with increased interactions with the physi-cian, the goals can converge. The patient is often besiegedby information and misinformation from various sources.As a result, an important component of continuing care isthe opportunity to continue a dialogue with the physicianso that the patient’s questions, level of understanding ofdiabetes care, and misconceptions can be addressed in away that would be beneficial to and protective of thepatient. For achievement of optimal results, a close work-ing relationship among the diabetes team members is mostuseful.

Where the arrangement is possible, a clinical endocri-nologist is most effective as the head of a comprehensivediabetes care program. Two reports have concluded that anendocrinologist’s involvement offers advantages in thecare, cost-effectiveness, and outcomes for patients withdiabetes (9,10). Educational programs alone have not beendemonstrated to improve major clinical outcomes, but pro-grams integrating both education and sophisticated, directcare of the patients have been effective. Optimally, theclinical endocrinologist should be the principal-care physi-cian for patients with either type 1 or type 2 diabetes.Alternatively, the clinical endocrinologist and the primary-care physician can comanage a program for their patientswith diabetes. Whatever the arrangement, the relationshipbetween the patient’s physicians should be collegial so thatthe particular roles of both specialist and generalist can beused to maximize the benefit to the patient.

Cost-Effective Comprehensive CareIntensive therapy has been shown to be cost-effective

in both type 1 and type 2 diabetes (9,10). Because two-thirds of the costs of diabetes management are currently

for inpatient care and complications of diabetes, clearlythe beneficial effects of intensive therapy on reducing boththe complications of diabetes and their progressionprovide strong support for the increased use of an inten-sive and comprehensive approach to diabetes care.

Although formidable barriers to the implementationof widespread, intensive programs of diabetes care stillremain, the benefits may be even greater in higher riskgroups, such as minority populations (6). It is reasonableto expect, and should be a goal, to have most patients withdiabetes in a community setting participate in an intensivetreatment program and achieve an excellent outcome(3,4,6).

SECTION 2: THE CLINICAL ENDOCRINOLOGIST IN CONTINUING CARE

Continuing CareThe patient with diabetes mellitus has a chronic but

highly treatable disease, which can have devastating andcostly complications. The health-care needs of such apatient are predicated on the control of the diabetes. Acomprehensive diabetes team approach yields the besthealth-care outcomes. The team approach, however,requires continuity of care and management.

The care of diabetes mellitus has become progres-sively more complex and demanding of both the patientand the physician. Comprehensive and intensive care ofdiabetes has been confirmed to yield important benefits bydelaying or preventing complications (1,3-5). For achieve-ment of these benefits, complex pharmacotherapeutic reg-imens, as well as insulin pumps or even pancreas trans-plantation, may be needed. The clinical endocrinologistcan best coordinate this complex continuing care toachieve the optimal outcome.

Thus, it is particularly critical for avoidance of com-plications that continuity of care be maintained for thedevelopment of long-term goals that can be shared andpursued by the patient, the physician, and other membersof the diabetes care team. When patients regularly shareinformation with the physician, the special training andknowledge of the clinical endocrinologist can help to iden-tify factors that may improve or disrupt diabetes control.For example, identification of improper habits can lead tothe formulation of solutions and the implementation ofbeneficial changes, such as alterations in diet and nutritionpractices, physical activity or exercise patterns, andresponses to stress in the environment; use and adjustmentof medications; careful attention to foot care; and adher-ence to a system of intensive diabetes self-management(11).

Intercurrent IllnessWhen the patient with diabetes needs to be hospital-

ized or has an intercurrent illness, the management of thepatient’s diabetes and of its effect on the course of theintercurrent illness often is the most important determinantof the outcome of the intercurrent illness (for example,infection, renal impairment, or hypertension). Therefore,

44 AACE Diabetes Guidelines, Endocr Pract. 2002;8(Suppl 1)

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the clinical endocrinologist can provide the patient withthe best care for the diabetes as well as ensure the mostfavorable outcome for the intercurrent illness (2).

Education and Preventive MeasuresDiabetes care is best focused on the prevention of

related complications and comorbid conditions, so thathospitalizations and cost of care are minimized. The mostcostly aspect of the care of diabetes is the hospitalizationsthat result from complications. The acute and chroniccomplications occur because of either the lack of under-standing in long-term and short-term control of the bloodglucose or the patient’s refusal to control the blood glu-cose levels. The educational responsibilities are shared bymany members of the diabetes care team, each of whomhas been specifically trained to understand and impart tothe patient the value of preventive measures (12). As aleader of the team, the clinical endocrinologist is able toeducate and train not only the patient but also other teammembers, as well as other physicians and nonphysicians,to understand and keep in mind the special needs of thepatient with diabetes and optimal management practices(12).

SECTION 3: NUTRITION AND EXERCISE

Nutrition and exercise are major interventions in thetreatment of diabetes mellitus. Their importance and effectin both type 1 and type 2 diabetes, however, have beeninadequately emphasized. The result has been unsatisfac-tory patient adherence.

With the introduction of an increasing number of oral-ly administered drugs for the treatment of type 2 diabetes,the focus has shifted to the use of these drugs rather thantackling the difficult problem of helping the patient imple-ment the necessary lifestyle changes for adherence tonutritional recommendations and exercise programs.

A recent study showed that newer pharmaceuticalagents cost, on the average, $1,700 per year per drug (13).In a recently completed survey of AACE member clinicalendocrinologists about prescribing practices for type 2diabetes, 90% of the 348 respondents reported pre-scribing three or more agents in combination to achievecontrol. Sixty-five percent used four agents in combina-tion. Of the survey participants, 95% reported that the oralcombinations currently available allow better glycemiccontrol than was ever achievable in the past. The problemsreported with use of drug combinations, however,included expense (75%), side effects (66%), monitoringdifficulties (61%), hypoglycemia (54%), and aversion topolypharmacy (30%) (14).

The notion of achieving blood glucose levels as nearnormal as possible in patients with type 2 diabetes is theunderlying prevailing goal for the clinical endocrinologist.The clinical endocrinologist views type 2 diabetes as aserious disease with potentially severe complications. Inpatients with type 2 diabetes, nutrition and exercise are

extremely important and the most cost-effective therapeu-tic interventions. The AACE System of Intensive DiabetesSelf-Management promotes the concept of the patientbeing in control and responsible for self-management. Animportant element in self-management of diabetesmellitus is the lifestyle changes necessary to adhere tonutrition and exercise programs.

In recent years, it has become clear that the prescrip-tions for diet and physical activity must be individualizedin order to improve patient adherence. The control overdietary intake and the effort to engage in physical activitycorrelates with the achievement of more normal blood glu-cose levels. The principles and strategies of nutrition andexercise for type 1 diabetes differ from those for type 2diabetes. Patients must understand and measure the effectof diet and physical activity in order to be expected toadhere to these necessary lifestyle changes. In type 2 dia-betes, nutrition and exercise can help maintain near-nor-mal blood glucose and optimal lipid levels, achieve desir-able weight, and improve physical condition.

Diet in Type 1 DiabetesWith use of insulin therapy for control of blood glu-

cose, the patient must understand the action and the dura-tion of the insulin being used as well as the effect of thetiming of the intake of food on the insulin action. It isunreasonable to expect the patient to maintain a constantmeal plan and insulin regimen. Flexibility of insulin dos-ing and timing must be taught to the patient. This flexibil-ity can be adapted by using the result of the blood glucosedetermination and the response to intake and timing offood. The DCCT demonstrated that patients who adjustedtheir food intake and insulin dosage in response to bloodglucose levels achieved lower glycosylated hemoglobinvalues than did the control group (15). The flexibilityempowered those patients to adhere more willingly. Theuse of carbohydrate counting to determine the appropriatebolus premeal dose of rapidly acting insulin has made theuse of intensive insulin therapy regimens even easier.

Diet in Type 2 DiabetesWeight loss and maintenance of weight loss result in

a decrease in the insulin resistance that is the hallmark ofmost patients with type 2 diabetes. Simply, a negativecaloric balance can decrease insulin resistance. The end-point does not have to be weight loss. In the process ofattaining a decrease in weight, blood glucose levels willimprove. By monitoring the blood glucose levels and thecaloric intake and output, the patient can understand theeffect of a negative caloric balance on the blood glucose.These measurements and observations will help promoteadherence. Patients do not have to achieve ideal bodyweight to improve control of blood glucose, control ofhypertension, and lipid levels. Loss of as few as 10 to 20lb (4.5 to 9 kg) will be helpful, but the weight loss mustthen be maintained and exercise programs must becontinued (16-18).

AACE Diabetes Guidelines, Endocr Pract. 2002;8(Suppl 1) 45

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Nutritional Composition of the DietNo clear-cut formula exists for carbohydrate, fat, or

protein intake in the patient with diabetes. The key is thecaloric intake relative to the caloric output. The motivationfor adherence to nutrition and exercise programs is thepatient’s understanding of the effect of these actions onblood glucose, blood lipids, and blood pressure (19).

Carbohydrate IntakeCurrently, the average amount of carbohydrate rec-

ommended for patients with diabetes is 55 to 60% of thetotal caloric intake. Little evidence is available to supportthe belief that sugar should be avoided or that starchesshould be preferred. Starches mixed with or containingfiber may slow down glucose absorption. Recently, starch-es (complex carbohydrates) have been shown to have ahigher glycemic index than such foods as milk, fruit, orsucrose (20).

Many starches are rapidly converted into 100% glu-cose during digestion. If the absorption is not sloweddown by a mixed meal containing fiber, the glycemicindex can be high. In contrast, sucrose is metabolized toglucose and fructose. Fructose has a lower glycemic indexthan does glucose because it has a slower rate of absorp-tion and is stored in the liver as glycogen (21).

The total amount of carbohydrate per meal, ratherthan its source, seems to be the critical factor thatdetermines its effect on blood glucose (22).

Fat IntakeNormal intake of fat should be limited to a maximum

of 30% of the total caloric intake. In patients with type 2diabetes, weight is usually a factor in developing a treat-ment program. Each gram of fat contains 9 calories, incontrast with 4 calories for each gram of carbohydrate orprotein. In overweight persons or those with dyslipidemia,fat intake should be reduced to as low as 15% of thecaloric intake. Again, an individualized approach, with thepatient making the choices through education, is the mosteffective means to achieve adherence (23). In persons withdyslipidemia, a concentrated effort should be made toavoid saturated fat and to substitute unsaturated fat ormonounsaturated fat. The content should be as low incalories and in fat as tolerated.

Ethnic, cultural, and financial barriers must be under-stood and considered by the physician and the diabetesself-management team as dietary plans are developed. Inaddition, careful monitoring of metabolic variables,including blood glucose, glycosylated hemoglobin, lipids,blood pressure, and body weight, and assessment of qual-ity of life as outlined in these guidelines are important.Monitoring serves to improve the patient’s ability toadhere to recommendations, maintain motivation, andsolve problems. It also enables the physician and the dia-betes self-management team to help the patient understandand adjust therapeutic interventions.

Protein IntakeIntake of protein should be 10 to 20% of the total

daily caloric intake. No evidence has indicated thatpatients with diabetes need a lower than average intake ofdietary protein to protect against the onset of renal disease(24). After the onset of microalbuminuria, every effortshould be made to decrease animal protein in the diet andto keep protein intake between 10 and 15% (25-27).

Use of AlcoholThe effect of alcohol on blood glucose in diabetes has

always been confusing. If possible, patients with diabetesshould avoid or limit the use of alcohol because predictingor anticipating its effect on blood glucose is difficult.

The effect on blood glucose depends not only on theamount of alcohol ingested but also on the amount of alco-hol ingested in relationship to food and the content of thefood consumed. Alcohol is oxidized by the liver. It mayimpair gluconeogenesis and result in subsequent hypo-glycemia. The hypoglycemia can be severe in personsreceiving injections of insulin because both insulin andalcohol can inhibit gluconeogenesis. Triglycerides canincrease in response to alcohol; thus, hyperlipidemia canworsen when alcohol is ingested (22,28).

In general, however, the effects of alcohol are notsevere. Because insulin is not required to metabolize alco-hol, no food group should be eliminated from the calculat-ed intake. Nevertheless, calories are added. Alcohol is cur-rently counted as a fat exchange.

Patients with pancreatitis, dyslipidemia, or neuropa-thy should especially avoid the use of alcohol (22).

Diet in Gestational DiabetesThe goal of therapy in patients with gestational dia-

betes is to maintain normal fasting blood glucose as wellas normal postprandial blood glucose leve975 letr 10slivl

-bete. EachndDietmjustbse ideivdquadized(and lftezeddurting)Tj 0.05 -11.75 TD 1.125 Tw (tve prgpres% of the prgnpanty to esuare areqnat, calorce)Tj 0.022 -11.75 TD1.6.68 Tw intake wit oue iap prpuriat,weighit tain orweighitlposland to avoid thedleveopmtent ofketoinuril (94).(Patientd)Tj 0.015 -12 TD 2.526 Tw with gestational di(betes areoAften dthetentiof thys arl)Tj 0.019 -11.75 TD 75061 Tw eduicated areqnatlly byia ulidiclo edocrtiologistd and thlbetes self-management teaa. Thys arlprtficuarllymotivcated by thairypeeceiedn responhiblitty tf

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glucose level of 250 mg/dL or higher at the time of exer-cise will experience a further increase in glycemia anddevelopment of ketosis.

The effects of exercise on the relationship of diet andinsulin have been well studied in type 2 diabetes and mustbe understood by the patient and the physician (33). Intype 2 diabetes, physical activity has been shown to helpdecrease peripheral insulin resistance, plasma triglyceridelevels, and very-low-density lipoproteins (VLDL).Because cardiovascular risk is high in most patients withtype 2 diabetes at the onset, the risk of cardiovascularcomplications with physical activity must be constantlyconsidered (34). Therefore, exercise must be viewed dif-ferently in type 2 diabetes than in type 1 diabetes.

In patients with either type 1 or type 2 diabetes, exer-cise can create a general sense of well-being. Exercise isgenerally credited with promoting physical fitness, whichin turn prevents or decreases the onset of cardiovasculardisease. Unfortunately, no controlled studies have beenconducted in patients with type 1 diabetes to prove thispoint (35). The Malmo study, however, demonstrated thevalue of intervention with physical activity and nutritionaltherapy in controlling the progression of type 2 diabetes(36). Exercise promotes flexibility and motor strength,which are also thought to promote a sense of well-being(37).

Principles of Exercise as Therapy in Type 2 DiabetesOf all patients with diabetes, 90% have type 2 dia-

betes. The major complication of type 2 diabetes ismacrovascular disease. There is now consensus that themacrovascular complications are attributable to the hyper-glycemia and the accompanying comorbid conditions ofhypertension and dyslipidemia (see Section 5).

Type 2 diabetes is usually the result of increasedinsulin resistance and eventual decrease in insulin secre-tion because of beta cell failure. Physical activityimproves blood glucose levels, the result of a decrease ininsulin resistance as well as weight loss. Insulin resistancehas been shown to decrease even without loss of weight.The increased sensitivity to insulin that results inincreased peripheral utilization of glucose occurs not onlyduring physical activity but for up to 48 hours after exer-cise (38). Therefore, exercise should be repeated at leastevery 48 hours to maintain this effect.

Any therapy that will reduce insulin resistance has thepotential to improve blood glucose control. Another bene-ficial effect of an exercise program is the promotion ofself-discipline necessary for controlling a chronic disease.Furthermore, in an era of increasing treatment options andcomplexity of orally administered medications for type 2diabetes, any therapeutic maneuver that decreases thecomplexity of treatment at low economic cost is cost-point (i-11.oimprolity ofhip5 -1VLDL0toases the ons2epeated at leHDLice2294and dysl -11neie. Unf1.75 TDae prohowel67 ro7Drth diabet9tributable to the beneimppshoiu.16015 -1 (seinueford1.75that.7575 TD 1.55 Tw (od glucosetributable to the bene)Tj 229.6ost isficiap. 027itous229, any theto i3.1ip Tw (i TD cr-ctiscipvels, the result of a Tc (incrTD 1.55 T-)durte5 TD 0.175 T TD 0 Tw (ficia 36.8443 0 TD 0.156 Tc sitivity 52Tj 39.64avoij 22.7he 46n)T (cel(im5 T-)du270.025 -11.75 96ctivgov)Tjexity of -)du6e )9tributa156 Tcca(resulturs873 esult of a 936 Tc (in)Tj -2 (imppshoiu.16015 -1suc TD fulord1.75tha. B ion )cise program is the pro39 t is -1subtlar.utomplexidy functy ow (imppul-2 rereaise (3l uinistered medicat2effectw646 u-224e)Taompasl ) TD 0 tased y -10.02 -11.75 TD 0..e progression of typntr309 t isP679 -1saise (3TD 1.55 T si.97ce

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glucose level with a surge of glucose output from the liver.The resulting hypoglycemia can be severe (40). If thepatient has poorly controlled diabetes, is poorly condi-tioned, and is stressed by the exercise, counterregulatoryhormonal output resulting from the stress induced byphysical activity along with the high blood glucose levelattributable to poor control of the diabetes can result in aneven higher blood glucose level (33).

The clinical endocrinologist and the diabetes self-management team can teach the patient all the variablesthat can result from exercise and, as part of the self-man-agement process, teach the patient to use the therapy ofphysical activity and conditioning to control the blood glu-cose level more effectively (33,34).

Effective blood glucose control can occur when thepatient learns to vary the dose of insulin appropriately,anticipate the need for intake of food before or afterphysical activity, and monitor the effect of the physicalactivity by appropriate blood glucose measurement afterparticipation in exercise. This monitoring is the responsi-bility of the patient. The responsibility of the physicianand the diabetes self-management team is to teach thepatient the principles and effects of physical activity andhelp make the patient a diabetes expert. In general, 15 g ofcarbohydrate should be added before or after physicalactivity, depending on the blood glucose level. If the activ-ity will be very strenuous, 30 g might be needed. Theanticipated effect of exercise and the regulation of thiseffect can and should be learned by the patient in order totake advantage of the benefits of exercise (37). In addition,the short-term and long-term effects of physical activitycould necessitate a decrease in insulin dosage. With thepatient gaining the experience of the effect of exercise,adjustment of the insulin dosage can result in more effec-tive control of the blood glucose level. The process ofphysical conditioning through exercise training can resultin a 20 to 30% decrease in the daily subcutaneous insulinrequirement (39).

SummaryNutrition and exercise programs are important, cost-

effective therapeutic maneuvers to assist patients withboth type 1 and type 2 diabetes achieve effective metabol-ic control. The patient must understand the effects andimportance of these therapeutic modalities in order to bemotivated to adhere to a beneficial nutrition and exerciseplan. The patient must be empowered not only to monitorthe blood glucose level but also to initiate the neededchanges in medication. When the patient becomes anactive participant in diabetes management, adherence toeffective therapy will increase and diabetes-related com-plications will decrease.

SECTION 4: PHARMACOLOGIC THERAPY FORTYPE 2 DIABETES

Major advances have occurred in the pharmacologictreatment of type 2 diabetes during the past 5 years in the

United States. Drugs in several new classes have beenapproved by the Food and Drug Administration, includ-ing the new biguanides, thiazolidinediones, meglitinides,α-glucosidase inhibitors, and new shorter acting insulin.In addition, new sulfonylureas and newer forms of avail-able sulfonylureas have been developed and approved. Allthese agents have tissue-specific sites of action to improveglycemia. They can be used in combination to take advan-tage of the respective mechanisms of action to reverse themultifactorial pathophysiology of beta cell dysfunction,insulin resistance, increased hepatic glucose production,and decreased peripheral glucose utilization.

The increase in choice and enhanced effectiveness ofthese new therapeutic compounds make possible theimproved control of blood glucose in patients with type 2diabetes. With this array of options, however, treatmentregimens have become increasingly complex and confus-ing. A trial-and-error approach is not acceptable. The useof these new drugs alone as monotherapy and in com-bination must be directed by the physician, preferably aclinical endocrinologist.

Type 2 diabetes is a serious disease in which severecomplications may occur, even in relatively asymptomaticpersons. Newly available drugs are quite effective. Ideally,to optimize the effect of these drugs, patients with diabetestaking them should become involved with the ongoingmanagement of their disease rather than simply taking thedrugs and assuming that they are “working.” By measur-ing the blood glucose at various times of day, the effect ofthe drug in relationship to activities such as meals, exer-cise, and stress can be judged. This information can lead tointelligent variations in therapy. Intensive diabetes self-management, as recommended by AACE, will improveblood glucose control and lower the glycosylated hemo-globin level. Only then will the risk of devastating andcostly complications of diabetes be reduced.

The cornerstones of therapy for type 2 diabetesremain proper nutrition, exercise, and education. Thesecomponents of care should be implemented at the outset ofthe diagnosis of type 2 diabetes. Many patients with type2 diabetes are immediately given medications without ini-tial optimal therapeutic use of a program of appropriatenutrition and physical activity. Frequently, this approachleads to a never-ending spiral of treatment with more andmore medication but little resulting improvement.

The choices of oral drug therapy for type 2 diabeteshave become extremely complex. The physician must bepositioned to use clinical judgment about the best combi-nations of drugs for the patient with diabetes. This discre-tion is particularly important in the long-term treatment ofa chronic disease that is unrelenting and progressive and inwhich the response to therapy changes over time.

The following material is a summary of informationabout pharmacologic options available for the treatment oftype 2 diabetes mellitus. See the current Physicians’ DeskReference (41) and package inserts (42-48) for detailedinformation about specific drugs and for additionalcomplete information.

48 AACE Diabetes Guidelines, Endocr Pract. 2002;8(Suppl 1)

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Sulfonylureas: ProfileSulfonylurea agents differ in potency, pharmacokinetics,and costUse as an adjunct to diet and exercise, not as a substituteMay be used as monotherapy or in combination with otherdrugs for diabetesMay be most useful in thin patients with insulinopeniaNot effective in type 1 diabetesNot to be used during pregnancyNot recommended for use in association with:

Major surgical procedures or general anesthesiaSevere infection, stress, or traumaPredisposition to severe hypoglycemia (for example,advanced liver or kidney disease)

Mode of ActionPrimary effect: stimulate insulin secretion by blocking theK+ channel of the beta cellSecondary effects: decrease hepatic glucose production;may improve insulin sensitivity at the receptor and postre-ceptor levels

ContraindicationsKnown hypersensitivity to the drugType 1 diabetes, diabetic ketoacidosisSulfa allergy

Potential Adverse EffectsHypoglycemia, hypersensitivity, weight gain

Metformin: ProfileMetformin (Glucophage) is a biguanide that has insulin-sensitizing propertiesMay be used as monotherapy or in combination with otherclasses of agents or insulinMay be most useful in obese patients with dyslipidemiaAssociated with no weight gain or mild weight loss

Mode of ActionPrimary effect: decreases hepatic glucose production byimproving insulin action at the liverSecondary effect: enhances muscle glucose uptake andutilization

ContraindicationsPatients prone to metabolic acidosis or hypoxic states,including renal failure, renal dysfunction with serum cre-atinine >1.5 mg/dL, liver failure, congestive heart failurerequiring pharmacologic intervention, diabetic ketoacido-sis, major surgical procedure, dye procedures (temporarilydiscontinue metformin therapy at time of intravascularadministration of iodinated contrast agent), sepsis,alcoholismUse with caution in patients >80 years old (age-relateddecline in renal function)

Potential Adverse EffectsLactic acidosis—extremely rare in properly selectedpatientsAnorexia, nausea, diarrhea—often transient

AACE Diabetes Guidelines, Endocr Pract. 2002;8(Suppl 1) 49

Table 1Commonly Used Sulfonylureas:

Dosage Data

Dailydose Doses/

Drug (mg) day

Glimepiride (Amaryl) 1-8 11 mg2 mg4 mg

Glipizide (Glucotrol) 2.5-40* 1-25 mg10 mg

Glipizide-GITS (Glucotrol XL)† 2.5-20 12.5 mg5 mg10 mg

Glyburide (Micronase, Diaβeta) 2.5-20 1-21.25 mg2.5 mg5 mg

Glyburide micronized (Glynase) 3-12 1-23 mg6 mg

*No further hypoglycemic effect at doses greater than 20mg/day.

†GITS = Gastrointestinal Therapeutic System (controlledrelease).

Adapted from DeFronzo RA. Current Management ofDiabetes Mellitus. Mosby-Year Book, 1998.

Table 2Metformin: Dosage Data

Daily dose Doses/Drug (mg)* day

Metformin (Glucophage) 500-2,550 2-3500 mg850 mg1,000 mg

*Begin with lowest dose and titrate, as needed, tomaximal dose (2,550 mg). Maximal benefit is usuallyseen at 2,000 mg.

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αα-Glucosidase Inhibitors: ProfileMay be used as monotherapy or in combination with sul-fonylureasEffectiveness demonstrated with all agents and insulinHigh rate of discontinuation because of gastrointestinaleffects but tolerated satisfactorily by some patientsProper titration of dosage is essentialMay be most useful in patients with exaggerated post-prandial increase in blood glucose

Mode of ActionAct locally in small intestine by inhibiting α-glucosidaseenzymes; this action slows digestion of ingested carbohy-drates, delays glucose absorption, and reduces the increasein postprandial blood glucoseGlucagon-like peptide is released because of delayedabsorptionSlight improvement in fasting blood glucoseModest reduction in glycosylated hemoglobin

ContraindicationsMajor gastrointestinal disorders, including inflammatorybowel disease, chronic ulceration, malabsorption, orpartial intestinal obstruction

Potential Adverse EffectsFlatulence, abdominal bloating—these effects maysubside over time

Thiazolidinediones: ProfileRosiglitazone (Avandia), and pioglitazone (Actos) havebeen approved for use. Troglitazone has been withdrawnfor use by the FDA.Rosiglitazone and pioglitazone can be used as monother-apy or in combination with sulfonylureas and metformin.Only pioglitazone is FDA approved for use in combina-tion with insulin therapy.May take several weeks for onset of action and severalmonths for “peak” actionRequire the presence of insulin for actionMay be most useful in patients with insulin resistance orazotemia

Mode of ActionPrimary effect: enhance tissue sensitivity to insulin inmuscle through activation of intracellular receptorsSecondary effect: suppress hepatic glucose productionNo stimulatory effect on insulin secretion

ContraindicationsKnown hypersensitivity or allergy to the drug or any of itscomponentsClinical evidence of active liver disease

Abnormal results of liver function tests:Troglitazone—alanine transaminase >1.5 times theupper limit of normalRosiglitazone—alanine transaminase >2.5 times theupper limit of normal

50 AACE Diabetes Guidelines, Endocr Pract. 2002;8(Suppl 1)

Table 3αα-Glucosidase Inhibitors: Dosage Data

Daily dose Doses/Drug (mg)* day

Acarbose (Precose) 75-300 3†50 mg100 mg

Miglitol (Glyset) 75-300 3†25 mg50 mg100 mg

*Begin with lowest dose (25 mg three times a day withmeals) and titrate at 2- to 4-week intervals, as needed,to maximal dose (100 mg three times a day withmeals).

†Take with first bite of each meal.

Table 4Thiazolidinediones: Dosage Data

Daily dose Doses/Drug (mg) day

Rosiglitazone (Avandia)† 2-8 1 or 22 mg4 mg8 mg

Pioglitazone (Actos)‡ 15-45 115 mg30 mg

†Initiate therapy at 4 mg/day.‡Initiate therapy at 15 mg/day.

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Pioglitazone—alanine transaminase >2.5 times theupper limit of normal

Congestive heart failure (New York Heart Associationclass III and IV)—unless benefit outweighs risk of volumeexpansion

Potential Adverse EffectsWeight gain (variable degrees), possibly related toimprovement in glycemic control and volume expansionWith troglitazone therapy, rare cases of severe idiosyn-cratic hepatocellular injury and necrosis

PrecautionsSerum transaminase levels must be assessed at start oftherapyFor troglitazone therapy, monitor liver function monthly for1 year and then quarterly thereafter—discontinue drug ifalanine transaminase is >3 times the upper limit of normalFor rosiglitazone therapy, monitor liver function every 2months for the first 12 months and then periodically there-after—discontinue drug if alanine transaminase is >3times the upper limit of normal on two samplesFor pioglitazone therapy, monitor liver function every 2months for the first 12 months and then periodically there-after—discontinue drug if alanine transaminase is 2.5times the upper limit of normal on two samples

Meglitinides: ProfileRepaglinide (Prandin), in the meglitinide class of benzoicacid derivatives, is an insulin secretagogueRequires the presence of functioning beta cellsCan be used as monotherapy or in combination withmetforminSimilarly, nateglinide is phenyladanine derivative, insu-line secretion

Mode of ActionPrimary effect: lowers blood glucose levels by stimulatingrelease of insulin in response to a glucose load (meal)Lowers both fasting and postprandial blood glucose buthas a greater effect postprandiallyThere are distinct beta cell binding sites for repaglinide/nateglinide apart from the sulfonylurea binding siteRepaglinide/nateglinide closes adenosine triphosphate-dependent K+ channels in beta cell membrane; the resul-tant increased calcium influx induces insulin secretion

ContraindicationsDiabetic ketoacidosis, with or without comaType 1 diabetesKnown hypersensitivity to the drug or its inactiveingredients

Potential Adverse EffectsHypoglycemia, hypersensitivity, weight gain

PrecautionsSimilar to those for sulfonylureas

AACE Diabetes Guidelines, Endocr Pract. 2002;8(Suppl 1) 51

Table 5Meglitinides: Dosage Data

Daily dose Doses/Drug (mg) day

Repaglinide (Prandin) 0.5-16* 2-4†0.5 mg1 mg2 mg

Nateglinide (Starlix)120 mg 360mg* 2-4†

*Taken 15 minutes before meals.†Based on number of meals.

Table 6Insulins: Available Types, Strengths,

and Duration of Action*

Available Duration ofDrug strengths action (h)

Regular U-100, 100 units/mL 3-6U-500, 500 units/mL

(Lilly only)Humalog U-100, 100 units/mL 1-2

(lispro)Novolog U-100, 100 units/mL 1-2

(insulin aspart)NPH U-100, 100 units/mL 18-24Lente U-100, 100 units/mL 18-24Ultralente U-100, 100 units/mL 24-36Lantus U-100, 100 units/mL 24

(glargine)50/50† U-100, 100 units/mL …70/30† U-100, 100 units/mL …75/25†† U-100, 100 units/mL …

*Daily dose and number of doses/day must beindividualized.

†NPH/regular mixture.††Lispro protamine suspension (NPL)/lispro pen, taken

15 minutes before the meal.

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SECTION 5: INTENSIVE TREATMENT OFCOMORBID CONDITIONS

Substantial evidence indicates that treatment ofcomorbid conditions is critically important for achievingoptimal outcomes in patients with diabetes mellitus.Cardiovascular disease accounts for 80% of mortality inpatients with diabetes mellitus. Therefore, control of otherrisk factors such as dyslipidemia, hypertension, renal dis-ease, obesity, and smoking is essential.

AtherosclerosisIn many patients, the first symptom of type 2 diabetes

is a myocardial infarction attributable to coronary arteryatherosclerosis. Atherosclerosis is well known to be asso-ciated with high plasma concentrations of cholesterol, par-ticularly low-density lipoprotein (LDL), whereas HDLcholesterol exerts a protective effect. Patients with uncon-trolled type 2 diabetes have dyslipidemia, characterized by

high triglyceride levels and VLDL, lowered HDL levels,and elevated LDL, especially small dense LDL. Becauseof the association of atherogenic small dense LDL withhypertriglyceridemia and the increase in atherosclerosis,patients with diabetes have an added risk that must be con-trolled. Additionally, lipid abnormalities and hypertensionare accelerated with the advent of early renal disease (seediscussion of lipids, obesity, and insulin resistance inSection 8 of these guidelines).

The lesions of atherosclerosis occur primarily in largeand medium-sized elastic and muscular arteries. The resultis insufficiency of the coronary, cerebrovascular, mesen-teric, and peripheral circulations. Patients with diabeteshave a high absolute risk for coronary mortality and mor-bidity and a worse prognosis than the general population.Furthermore, women with diabetes mellitus lose their rel-ative protection against coronary artery disease.Aggressive treatment, in accordance with the NationalCholesterol Education Program guidelines, is advised

52 AACE Diabetes Guidelines, Endocr Pract. 2002;8(Suppl 1)

Table 7Fasting and Postprandial Blood Glucose and Glycosylated Hemoglobin Responses

to Pharmacologic Treatment in Patients With Type 2 Diabetes*

Decrease in 1-hour PPBGfasting BG ( from baseline) HbA1c

Drug (mg/dL) (mg/dL) ( from baseline)

Sulfonylureas 40-60 … 1.0-2.0%

Repaglinide/Nateglinide 30.3 56.5 1.1%

Metformin 53 … 1.4%

Rosiglitazone (across dose range) 25-55 … 0.1-0.7%

Pioglitazone 20-55 … 0.3-0.9%

α-Glucosidase inhibitors 20-30 20-74 0.5-1.0%

*BG = blood glucose; HbA 1c = glycosylated hemoglobin; PPBG = postprandial blood glucose.

Clinical Expectations

Table 8Effect of Pharmacologic Treatment of Type 2 Diabetes on

Insulin Secretion and Glucose Production and Uptake

Hepatic PeripheralInsulin glucose glucose

Drug secretion production uptake

Sulfonylureas or repaglinide Increase Slight decrease Slight increase

Metformin No change Decrease Mild increase

Pioglitazone or rosiglitazone No change Mild decrease Increase

α-Glucosidase inhibitors No change No change No change

Insulin Decrease Decrease Increase

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(23). Most myocardial infarctions may be caused bylesions that are considered hemodynamically insignifi-cant. Therefore, additional maneuvers such as plaque sta-bilization (with use of aspirin or angiotensin-convertingenzyme [ACE] inhibitors) may be important.

DyslipidemiaAlthough numerous clinical studies have demonstrat-

ed the beneficial effects of lipid-lowering agents, no pub-lished clinical trials have assessed the protective effect oflipid-lowering agents on coronary artery disease exclu-sively in patients with diabetes. Analysis of subgroups ofpatients in several large studies, however, provides evi-dence of improved outcomes, especially in patients withdiabetes. These investigations include the Helsinki HeartStudy (49), the Scandinavian Simvastatin Survival Study(“4S”) (50), the Cholesterol and Recurrent Events (CARE)Trial (51), and the Air Force/Texas Coronary Atheroscle-rosis Prevention Study (52). From these studies, one couldextrapolate the conclusion that intensive therapy fordyslipidemia would be as protective as for the generalpopulation. AACE believes that intensive treatment ofdyslipidemia in patients with diabetes is important andnecessary for protection from the macrovascular compli-cations of dyslipidemia.

Currently, four major classes of lipid-lowering drugsare available:

1. Statins (hydroxymethylglutaryl-coenzyme A reductaseinhibitors): lovastatin, simvastatin, pravastatin, fluva-statin, and atorvastatin

2. Fibric acid derivatives: gemfibrozil, fenofibrate3. Bile acid sequestrants: cholestyramine, colestipol4. Nicotinic acid (which should be used with extreme

caution, if at all, in patients with diabetes because ofdeleterious effects on glycemic control)

The most common lipid abnormality in patients withtype 2 diabetes mellitus is hypertriglyceridemia (53). Therelationship between hypertriglyceridemia and coronaryartery disease is complex. A recent meta-analysis suggest-ed that triglyceride levels are an independent risk factorfor coronary artery disease (54). Triglyceride-rich lipopro-teins tend to be associated with low HDL cholesterol lev-els and small dense LDL particles. This lipid triad is oftenassociated with insulin resistance, hypertension, andprethrombotic states.

HypertensionRecently, the UKPDS (55) demonstrated that inten-

sive control of blood pressure in patients with hyperten-sion reduced all diabetes complications by 24%, diabetes-related deaths by 32%, strokes by 44%, heart failure by56%, and microvascular complications by 37%. Forachieving control of hypertension, β-adrenergic blockingagents and ACE inhibitors were equally efficacious.

ACE inhibitors may confer an additional benefit.Studies have shown a specific effect of ACE inhibitorsslowing the progression of diabetic nephropathy in

patients with type 1 and type 2 diabetes (56). ACEinhibitors also may slow the progression of microalbu-minemia to macroalbuminemia, even in normotensivepatients with type 2 diabetes (57). Recently, anotherpotential beneficial effect of ACE inhibitors has beenreported. Endothelial dysfunction is common in patientswith type 2 diabetes. ACE inhibitors have been shown toimprove endothelial function in type 2 diabetes (58). Otherrenal protective measures include prevention and prompttreatment of urinary tract infections, institution of a low-protein diet, and avoiding or minimizing the use ofradiographic contrast media.

In its sixth report, the Joint National Committee onPrevention, Detection, Evaluation, and Treatment of HighBlood Pressure (59) concluded that systolic blood pressureshould be reduced below 130 mm Hg and diastolic bloodpressure below 85 mm Hg to achieve optimal riskreduction.

Patients with type 2 diabetes and hypertension shouldmonitor their blood pressure frequently with home bloodpressure self-monitoring. Blood pressure can vary withfood and salt intake, stress, and weight gain. Patientsshould be taught how to judge the effect lifestyle changesmight have on the blood pressure and when to adjust theirlifestyle in addition to their medication. The physician andthe diabetes self-management team should empower thepatient to be aware of these fluctuations. The team shouldteach the patient the significance of reducing the risk com-plications of hypertension and the importance of the dataobtained with home blood pressure self-monitoring.

Cardiovascular DisordersAntioxidants such as vitamin E have been shown to

decrease the incidence of myocardial infarction. In con-trast, β-carotene has been ineffective in decreasing theincidence of myocardial infarction. Prevention of vascularevents by the antiplatelet effect of daily low-dose aspirin(as low as 30 mg/day) has been well established. Dailylow-dose aspirin therapy is important for both primary andsecondary prevention of cerebral and cardiac events (60).Less well established is the proposal to use multivitaminpreparations containing folate, vitamin B12, and vitaminB6 to reduce the blood level of homocysteine, a knownatherogenic agent (61,62). Outcomes of myocardialinfarction (7,63,64) and stroke improve with near-normal-ization of the blood glucose level.

Screening for asymptomatic coronary artery disease isan important consideration in patients with diabetes(65,66). An appropriate protocol for such screening hasnot been adequately tested. Increasing age, gender, cardio-vascular risk factors, microalbuminuria, and retinopathymay identify high-risk groups for whom such testing isindicated.

OverallOptimal care of the patient with diabetes must include

intensive glycemic control, proper nutrition, a physicalactivity program, cessation of smoking, and weightcontrol. Aggressive medical management of comorbid

AACE Diabetes Guidelines, Endocr Pract. 2002;8(Suppl 1) 53

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conditions, such as dyslipidemia, hypertension, and earlyrenal disease, and use of antiplatelet therapy for preven-tion of vascular events are critical to improved outcomesand decreased cost of care for diabetes and its complica-tions.

SECTION 6: COST AND COST-EFFECTIVENESSOF DIABETES CARE

The cost of diabetes mellitus is enormous, not only interms of human morbidity and mortality but also relativeto the economic burden it has imposed on the health-caresystem in the United States. Although patients with dia-betes constitute only 3.1% of the total US population, theyincur 11.9% of the total US health-care expenditures (67).

Factors Contributing to CostsThe economic costs of diabetes consist of direct

health-care expenditures as well as the loss of productivi-ty because of related disability and premature death. Thedirect medical costs of diabetes may be calculated as bothmedical expenses attributable to diabetes and total medicalexpenditures incurred among patients with diabetes. In1997 in the United States, direct medical expendituresattributable to diabetes totaled $44.1 billion. This overallamount consisted of $7.7 billion for diabetes and acuteglycemic care, $11.8 billion due to the excess prevalenceof related chronic complications, and $24.6 billion due tothe excess prevalence of general medical complications.Analysis of cost categories showed that 62% of costs werefor inpatient care, 25% were for outpatient services, and13% were for nursing home care. In addition, indirectcosts included $17 billion from premature mortality and$37.1 billion from disability, a total of $54.1 billion (68).

Comparative Medical ExpendituresIn 1997, total medical expenditures in the United

States for people with diabetes were $77.7 billion or$10,071 per capita, in comparison with $2,669 per capitafor those without diabetes (68). For 1992, Rubin and asso-ciates (69) reported similar figures of $9,493 and $2,604,respectively, and noted that 15% of the national health-care expenditures were spent on treating the 10.3 millionpeople with overt diabetes. It has been estimated thatanother 5.4 million people have undiagnosed diabetes, afactor that would further increase the estimates of health-care costs for those with diabetes (70).

Effectiveness of Intensive ManagementSince the publication of the findings of the DCCT (1)

and, more recently, of the UKPDS (3,4), it has becomeclear that tighter control of blood glucose in both type 1and type 2 diabetes can result in significant reduction inthe development and progression of microvascular com-plications of diabetes. Furthermore, the frequency ofmacrovascular complications is decreased by near-nor-malization of the blood glucose levels. Multiple contribut-ing causative factors of macrovascular complications,including dyslipidemia and hypertension, make the

statistical correlation between blood glucose andmacrovascular complications less definite; nonetheless,they are associated variables.

Although the intensive management of diabetes,which is necessary for achievement of tighter blood glu-cose control, is associated with higher “up-front costs” oflabor, medications, and supplies, this investment has beenshown to be effective in reducing morbidity and mortalityas well as minimizing later expenditures for the most cost-ly long-term complications (10,71,72). The cost benefit oftight glucose control is most pronounced in young patientswho, in general, will have a longer subsequent duration oflife during which the complications of diabetes coulddevelop if normoglycemia is not achieved (10).

The cost of treating diabetes with “intensive” therapywithin the DCCT ($4,014/yr) was 2.4 times that of “con-ventional therapy” ($1,666/yr). This cost was in a researchsetting. Inpatient initiation of treatment during the studyaccounted for more than 80% of the additional cost (73).Outside the DCCT study participants, in physician prac-tices, however, intensive therapy was much less expen-sive—only $2,337/yr (67). This difference was primarilydue to less frequent and less prolonged use of hospital ser-vices and a lower cost for outpatient visits. Dedicated dia-betes management teams led by an endocrinologist havebeen shown to maintain DCCT-level control of diabeteswhile using fewer inpatient and emergency departmentresources (74).

A simulation model of disease progression and costs(75) revealed that intensively treated patients with dia-betes live 5.1 years longer than those given conventionaltherapy, with a lifetime increment in cost of only $33,746or $6,616 per year of additional life. Therefore, the inten-sive treatment represented an extremely cost-effectiveinvestment. In addition, with further consideration of thereduction in complications (blindness, end-stage renal dis-ease, and lower extremity amputation) that decrease thequality of life, the study noted that the incremental cost per“quality-adjusted life year” gained was only about$20,000 for type 1 diabetes and $16,000 for type 2diabetes—relatively inexpensive in relationship to othercommonly accepted medical therapies.

Short-term outcome analysis (76) has shown thatimproved glycemic control in patients with type 2 diabetesis associated with improved quality of life, higher retainedemployment, greater productive capacity, and less absen-teeism. When these factors are considered, the cost ofintensive therapy seems offset by even greater economicbenefit, not only to the individual patient but to society asa whole.

In the UKPDS (55), tight control of blood pressurewas shown to confer additional preventive benefit.Although this effort increased the average cost of drugs by£ 613 ($977 US equivalent), a decrease in complicationsnecessitating hospitalization accounted for a reduction of£ 700 ($1,116 US equivalent). Tight control was estimat-ed to cost less than £ 3,000 ($4,784 US equivalent) peryear of life gained. Thus, intensive diabetes managementmakes as much sense economically as it does medically.

54 AACE Diabetes Guidelines, Endocr Pract. 2002;8(Suppl 1)

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Numerous studies have documented the importance ofa diabetes management team led by a clinical endocrinolo-gist in achieving the tight blood glucose control necessaryto yield the benefits of reduction in human pain and suffer-ing. Such studies have demonstrated the cost efficiency ofthis approach to diabetes care in reducing the frequency ofunnecessary visits to the emergency department and shorthospital stays (74), in decreasing the duration of hospitalstay for patients with diabetes (2), in treating diabeticketoacidosis more efficiently (77-80), and in providingongoing care to patients with diabetes that reduced bothcardiovascular and renal morbidity and mortality (6).

SECTION 7: PATIENT AND PHYSICIANRESPONSIBILITIES FOR EFFECTIVE DIABETES CARE

In any therapeutic situation, the physician and thepatient have specific responsibilities. During the past 3decades, this concept of shared responsibility has espe-cially been emphasized in the management of chronic dis-eases, and type 1 diabetes mellitus is a notable example.

Until recently, type 2 diabetes mellitus had not beenperceived as being a serious disease, perhaps becausepatients with type 2 diabetes may be relatively asympto-matic. The medical community now knows that eventhough the patient may be asymptomatic, a high blood glu-cose level will result in unrelenting development of bothmicrovascular and macrovascular disease. The microvas-cular disease leads to ophthalmologic, neurologic, andrenal complications. The comorbid conditions of dyslipi-demia and hypertension have a complex relationship withdiabetes. They may be worsened by poorly controlled dia-betes or, in some settings, may be a direct result of lack ofglycemic control. To achieve glycemic control, theasymptomatic patient with type 2 diabetes must becomean active participant in the management of the blood glu-cose level. The physician and the diabetes managementteam must teach, nurture, and continually guide the patienttoward self-management of the blood glucose.

The AACE Medical Guidelines for the Managementof Diabetes Mellitus include a patient-physician contract.This contract outlines both the patient’s and thephysician’s responsibilities in the management of this veryserious and complicated disease. The summarizedresponsibilities of each stakeholder follow.

The Patient’s Responsibilities1. Perform monitoring of blood glucose consistently to

help understand the dynamics of blood glucose changesrelative to medication, diet, stress, and exercise.

2. Understand the importance of smoking cessation indecreasing the risks of diabetes-related macrovascularand microvascular complications and, if a smoker,enroll in a program of smoking cessation.

3. Learn the importance of participation in a program ofprescribed exercise for weight reduction and physicalconditioning.

4. Know the importance of and reasons for the consistentuse of aspirin in helping to reduce the risk of macro-

vascular complications. This knowledge will aid inincreasing adherence to recommendations.

5. Monitor blood pressure consistently to help regulate theblood pressure and blood pressure medication. Under-stand the effects of medication and stress on blood pres-sure control and the risk of the lack of blood glucosecontrol. This understanding will encourage adherence toblood pressure monitoring and control measures anddecrease the risk of complications from hypertension, aserious comorbid complication of diabetes.

6. Recognize and understand the psychologic barriers thatprevent adherence to the system of intensive self-man-agement of diabetes. Learn how to express feelings anddefine the barriers to expressing feelings to the physi-cian and the self-management team. This skill mighthelp increase adherence with the system of intensiveself-management of diabetes.

7. Learn the best techniques of foot care management andmake a commitment to intensive foot care.

8. Understand the reasons for the onset of retinopathy, andrecognize the signs and symptoms for early detection.

9. Understand the need for establishing goals for blood glu-cose, lipids, and blood pressure. Learn to participate inthe development of these goals and in their modification,in consultation with the physician. After the goals havebeen established, develop a dedication to reaching thosegoals through intensive self-management of diabetes.

10. Actively participate in continuing diabetes education,such as support groups and physician and educatorinteractions, between regularly scheduled appointments.Share this valuable resource, becoming a teacher toother patients with diabetes and thereby learning fromsuch interactions.

11. Adhere to proper nutrition and physical activity pro-grams. Understand the physiologic rationale for theireffectiveness. To improve adherence, discuss barrierswith the physician and the diabetes management team.

12. Accurately document serial blood glucose and bloodpressure measurements. Understand that the purpose ofkeeping such records is to help clarify blood glucoseand blood pressure relationships to dietary aberrations,stress, exercise, and acute illnesses such as infections.This documentation will facilitate appropriate changesin treatment.

13. Understand the importance of keeping regularly sched-uled appointments. Effective treatment of diabetesdepends on a continuum of care, including periodicmedical consultations.

14. Adhere to the proper use of medications. Understandingthe mechanism of action of the medication will enhanceadherence. If changes in the medication seem necessary,learn to communicate with the physician betweenappointments so that appropriate alterations can bemade as a collaborative effort with the physician.

15. Understand the meaning of glycosylated hemoglobin,and know the results of personal glycosylated hemoglo-bin values.

16. Appreciate that the patient-physician contract is a tool tohelp both the patient and the physician uphold theircommitments in the therapeutic plan.

17. Evaluate the compliance of the physician, and commu-nicate this assessment to the physician.

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The Physician’s ResponsibilitiesFor an effective diabetes self-management system,

the physician must also fulfill the following responsibili-ties in the patient-physician contract.

1. Adhere to the protocol outlined in the AACE MedicalGuidelines for the Management of Diabetes Mellitus: ASystem of Intensive Diabetes Self-Management.

2. Appropriately collect the patient data (details of theclinical course and the laboratory findings) so that clin-ical outcomes can be measured and related to economicoutcomes.

3. Determine patient satisfaction and quality of life by useof questionnaires at yearly intervals.

4. Utilize a system of communication and documentationof the communication with the diabetes self-manage-ment team so that the team is truly an extension of thephysician’s care.

5. Utilize diabetes skill evaluation programs, and objec-tively evaluate the patient semiannually.

6. Define the frequency of patient visits, and assess thepatient’s ability and desire to adhere to the system ofintensive diabetes self-management.

7. Document, evaluate, and rate the patient’s concernsevery 3 months in a utilizable data format. As the keyelement, the patient must feel comfortable describingbarriers to intensive self-management. The patientshould always be the focus of the diabetes self-manage-ment team.

8. Evaluate the effectiveness of the documentation of careof the patient. Pay particular attention to the quality ofthe documentation; continuous improvement in thequality of documentation should be an integral part ofthe system of care.

9. Supervise the education of the patient. The physicianmust be involved in discussing preventive methods andexplaining risk reduction so that the patient gains exper-tise in diabetes management and is encouraged by theentire diabetes care team.

10. Ensure that the patient understands and adheres to pre-ventive measures, including detailed instructions forfoot care, diet, and physical activities, aimed at reducingthe risk of complications.

11. Utilize a process to evaluate the patient’s adherence tothe system of intensive self-management. The assess-ment should be objective and amenable to evaluation inquery format related to other variables. The programshould include mechanisms to determine whether thepatient is taking medicines and insulins safely and cor-rectly. A continuing program should be undertaken toidentify errors and misconceptions as well as to educateothers in the system who help care for these patients.This effort will reduce the frequency of potential mis-takes in the overall process.

The Patient-Physician ContractIn medical care, the social contract is between the

patient and the physician. Both the physician and thepatient have obligations in this therapeutic relationship.The fulfillment of those obligations and responsibilities byeach party is critical to achieving near-normal blood glu-cose levels. In patients with type 1 or type 2 diabetes,decreasing the rate of complications, enhancing the quali-ty of life, limiting the associated morbidity, and minimiz-ing the economic costs can be achieved by increasingadherence and attaining near-normalization of the bloodglucose levels.

56 AACE Diabetes Guidelines, Endocr Pract. 2002;8(Suppl 1)

Table 9Summary of Patient and Physician Responsibilities

in Intensive Diabetes Self-Management System

Patient responsibilities Physician responsibilities

Monitoring of blood glucose Adherence to the system of intensive self-managementExercise program of diabetesAdherence to dietary guidelines Measurement of outcomesBlood pressure monitoring Determination of patient satisfactionSmoking cessation Maintenance of communication with teamConsistent use of aspirin Development of evaluation programs; include safety inOvercoming psychologic and other barriers taking medication and identification of patientHealthy expression of feelings misconceptionsFoot and eye care Listening to patient concernsUnderstanding “targets” for control of blood glucose Establishing and maintaining follow-up schedule

and blood pressure Documentation of patient careCommunication with physician and diabetes care team Supervision of the patient’s diabetes educationKeeping appointments Encouragement of patient in use of preventive measuresRecord keeping and risk reductionAdherence to medication regimen Supervision of proper foot care proceduresEvaluation of physician and diabetes care teamTreating and modifying “targets” in collaboration

with physicianKnowledge of personal glycosylated hemoglobin

value and its meaning

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SECTION 8: THE INSULIN RESISTANCE SYNDROME

CharacterizationThe insulin resistance syndrome is characterized by

glucose intolerance, hypertension, dyslipidemia, and vis-ceral obesity (81,82). All of these findings are risk factorsfor ischemic heart disease, but insulin resistance, asassessed by the fasting insulin level, has itself been shownto be an independent risk factor for ischemic heart diseasein investigations such as the Quebec Heart Study (83). Infact, in that study, insulin resistance was shown to be amore important risk factor than total apolipoprotein B orHDL cholesterol levels.

The dyslipidemia associated with insulin resistance ischaracterized by a high triglyceride level and a low HDLcholesterol level. In the atherogenicity of the dyslipidemiaassociated with insulin resistance, however, small denseLDL particles, postprandial hyperlipidemia, and increasedremnant particles may be equally important factors(81,84).

Associated ConditionsInsulin resistance as a cause of hypertension is more

prevalent in some ethnic minority groups than in others.The mechanism for the increased prevalence of hyperten-sion is related to higher insulin levels acting on the renaltubule, increased reabsorption of sodium, and vasocon-striction through stimulation of the sympathetic system byinsulin (85). In addition, the insulin resistance syndrome isassociated with endothelial dysfunction (82,86), leading toa decrease in production of nitric oxide. The decreasedproduction of nitric oxide, in turn, leads to vasoconstric-tion and stimulation of clotting factors, platelet aggrega-tion, and decreased breakdown of fibrinogen throughstimulation of plasminogen activator inhibitor. Endo-thelial dysfunction is also associated with increasedendothelial permeability to molecules such as lipoproteins.In addition, activation of growth factors leads to accelerat-ed atherosclerosis. Abnormal endothelial permeability isalso present in the glomerulus, in reality an arteriole, lead-ing to microalbuminuria and proteinuria. The level of pro-teinuria has been shown to be inversely proportional to theinsulin sensitivity. In patients who are at high risk for dia-betes because of insulin resistance, proteinuria will oftenbe detected before fasting or postprandial blood glucoselevels are found to be high.

Overt diabetes will develop when insulin productioncannot be increased to overcome insulin resistance. Incomparison with thin patients, many obese patients with-out diabetes produce 5 to 8 times more insulin—anamount that can be as much as 500 U/day—to overcomeinsulin resistance. Thus, type 2 diabetes can be attributedto a genetic failure of the pancreatic beta cells to compen-sate for insulin resistance (87). The presence of hyper-uricemia, with or without clinical manifestations of gout,is also a feature of the metabolic syndrome which includesinsulin resistance. Therefore, patients known to havehypertension, dyslipidemia, hyperuricemia, or gout at an

early age should undergo periodic assessment for the pres-ence of diabetes.

Some evidence suggests that breast cancer may beassociated with insulin resistance—because of stimulationof tumor growth by high insulin levels or by decreasedhepatic production of sex hormone-binding globulin andhigher free estrogen levels (88). Moreover, many cases ofpolycystic ovary disease are associated with insulin resis-tance. High insulin levels stimulate the production ofandrogens from the ovaries and adrenal gland and luteiniz-ing hormone from the pituitary gland (89). The decreasedsex hormone-binding globulin further increases the freeandrogen levels and increases the likelihood of manifesta-tions of the disease (acne, hirsutism, virilism, amenorrhea,and infertility). Women with polycystic ovaries, becauseof their underlying insulin resistance, are at high risk forsubsequent development of the other manifestations ofpolycystic ovary disease including diabetes mellitus andvascular disease.

Causative FactorsInsulin resistance is a state in which insulin-sensitive

tissues, such as skeletal muscle, have a reduced sensitivi-ty to the effects of insulin on glucose uptake. At least 50%of any patient’s insulin resistance is due to genetic factors.Insulin resistance is worsened by aging, inactivity leadingto a loss of muscle mass, and the development of obesity.For obesity to be associated with insulin resistance, it mustbe of the android or male distribution (that is, with a highwaist-to-hip ratio) and not the gynoid or female distribu-tion, with most of the adipose tissue in the lower body (adecreased waist-to-hip ratio). Furthermore, subcutaneousadipose tissue is not associated with insulin resistance,whereas intraperitoneal or visceral adiposity is. The ratioof intraperitoneal to subcutaneous fat can be determinedby computed tomographic scanning or magnetic reso-nance imaging. Increased intraperitoneal fat is suspected ifthe waist circumference is more than 37 inches (94 cm) orthe waist-to-hip ratio exceeds 0.85 in women or 1.00 inmen (82,90).

Other environmental factors that increase insulinresistance are cigarette smoking and a lack of exercise.Insulin resistance is lowered by a moderate alcohol intake(one to two drinks per day); however, AACE does notadvocate the use of alcohol to achieve such a result.Pharmacologically, drugs such as nicotinic acid, β-adren-ergic blocking agents, thiazide diuretics, progesterones,and short-acting dihydropyridine calcium channel block-ers increase insulin resistance, whereas ACE inhibitors,angiotensin II receptor blockers, and estrogen replacementtherapy lower insulin resistance.

Because infections and cancers may exacerbate theinsulin resistance syndrome, investigators have postulatedthat the final common pathway of the insulin resistancesyndrome is through the action of cytokines. Althoughmany cytokines have been shown to be increased in theinsulin resistance syndrome, the cytokine that could mostreasonably be the link among all the manifestations of thesyndrome is tumor necrosis factor-α.

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TreatmentThe key to nonpharmacologic therapy to reduce

insulin resistance is increased physical activity anddecreased caloric intake. Both the increase in physicalactivity and the decrease in caloric intake will increaseinsulin sensitivity, with or without weight loss (91).

As little activity as walking for 40 minutes four timesper week is enough to lower insulin resistance. Likewise,as little physical activity as walking 5 miles per week canreduce the risk of developing diabetes by 6% (the reduc-tion is even more in obese persons and those persons witha family history of diabetes) (36,92). Exercise increasesthe affinity of the insulin receptor for insulin, increases themobilization of glucose transporters, and increases theactivity of tyrosine kinase, each of which will lead to adecrease in insulin resistance in skeletal muscle. By pref-erentially decreasing intraperitoneal adiposity, increasedactivity also results in a decrease in free fatty acids and afurther decrease in insulin resistance. Similarly, even aslittle as a 5% decrease in body weight will result in asubstantial reduction in insulin resistance.

When the plasma glucose is high in the patient withdiabetes, insulin resistance is increased. Irrespective of themethod used to lower blood glucose levels, reversal of“glucotoxicity” will result in a decrease in insulin resis-tance as well as an increase in endogenous production ofinsulin.

SECTION 9: AACE SYSTEM OF INTENSIVEDIABETES SELF-MANAGEMENT

The AACE System of Intensive Diabetes Self-Management is divided into three phases. Phase I providesthe opportunity for the initial patient assessment. Initialpatient education and formulation of a customized thera-peutic approach may require several outpatient visits dur-ing a period of a few weeks. Phase II, the follow-up phase,provides for interim assessments of the patient’s physicalcondition, reaction to intensive therapy, and understandingof the tools for diabetes self-management. Phase III con-sists of the ongoing assessment of the complications ofdiabetes mellitus as well as reeducation of the patient andencouragement to maintain enthusiasm for the difficulttask of intensively managing blood glucose levels.

In this ongoing system, the patient-intensive partici-pation is the key to effective control of the diabetes. Theclinical endocrinologist or other physician and all mem-bers of the health-care team must facilitate this participa-tion by the patient.

Phase I: Initial Assessment

The primary goal of Phase I is the assessment of thepatient’s disease status and risk factors for complicationsof diabetes. This goal may be accomplished by a thoroughelicitation of the patient history, performance of a com-plete physical examination by the physician, and appropri-ate laboratory evaluation. During Phase I, which mayrequire multiple patient visits during an interval of 3 to 4

weeks, the physician will gather information, develop ini-tial recommendations for the patient, and begin a diabetesself-management program with the help of the diabeteshealth-care team. The educational program should addressappropriate nutrition, exercise, medication, record-keep-ing systems, and self-monitoring of blood glucose. As thepatient begins to understand the rationale for intensivecontrol of blood glucose, the regimen can be modified andthe patient can be taught the reasons for modification. Atthis time, the clinical endocrinologist can schedule theappropriate evaluations or referrals for assessment of com-plications and specific risk factors.

Other goals during Phase I are to assess the patient’sknowledge base about diabetes mellitus and to evaluatethe ability of the patient to learn new skills and techniques.These assessments can be done by using a combination ofobjective knowledge tests, psychologic adjustment tests,and interview questions. After these assessments havebeen completed, the physician and other team membersshould be able to initiate the appropriate level of educationregarding diabetes self-management skills.

During Phase I, the physician should evaluate thepatient’s commitment to a program of intensive treatmentof diabetes and elicit the patient’s written agreement toparticipate in the diabetes self-management system. Thephysician, patient, and health-care team should develop aset of individualized instructions for the patient’s care.

Patient HistoryThe patient’s responses to the following areas of

questioning should help the physician confirm the diagno-sis and duration of diabetes mellitus, establish the successor failure of previous treatment regimens, evaluate thepresence of existing complications of diabetes, and deter-mine the patient’s risk for the future development ofcomplications (93).

1. What is the patient’s chief complaint?How long has the patient had diabetes?

2. Did onset of diabetes include the following:a. Polydipsia?b. Polyuria?c. Polyphagia?d. Unexplained weight loss or gain?

3. Is there a family history of diabetes or otherendocrine disorders?

4. Does the patient have a history of gestational dia-betes?a. Hyperglycemia?b. Delivery of an infant weighing >9 lb (4.1 kg)?c. Toxemia?d. Stillbirth?e. Other complications of pregnancy?

5. Has the patient lost or gained weight? What is thepatient’s current nutritional regimen?

6. What are the patient’s exercise history and ability toexercise?

7. What are the patient’s current non-diabetes-relatedmedications?

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8. What is the patient’s alcohol intake?9. Is there a history of recreational drug use?

10. Has the patient ever been hospitalized or undergonea surgical procedure?

11. If the patient has already been diagnosed as havingdiabetes mellitus:a. When and how was the diabetes diagnosed?b. Which medications have been used to treat the

diabetes, and in which order? Establish thecurrent treatment regimen, including nutritionand exercise programs.

c. How have the patient’s blood glucose levels beenmonitored in the past? Has the patient monitoredblood glucose at home? How frequently was thepatient’s glycosylated hemoglobin monitored?Were the results of these tests used to maximizethe degree of control of diabetes?

12. Does the patient have symptoms of any of thefollowing types of complications of diabetes?a. Ophthalmologic (including retinopathy)?b. Neuropathy?c. Renal?d. Vascular (cardiovascular, cerebrovascular,

peripheral vascular system)?e. Sexual dysfunction (men and women)?f. Ketoacidosis?g. Hypoglycemia?h. Infections (for example, cutaneous, foot, gyneco-

logic)?13. Does the patient have any identifiable risk factors

for complications of diabetes?a. Family history of diabetes or coronary artery

disease?b. Hypertension (systolic, diastolic)?c. Smoking history?d. Lipid abnormalities?e. Central obesity?

Physical ExaminationPhase I should include a complete physical examina-

tion of each patient. Special attention should be directed tothose aspects of the examination that focus on specificareas of risk for the patient with diabetes (93), includingthe following factors:

1. Height and weight measurements2. Blood pressure determination, including orthostatic

evaluation3. Ophthalmoscopic examination4. Thyroid palpation5. Cardiac examination6. Evaluation of pulses, including carotid pulses or

bruit and respiratory variation7. Foot examination8. Skin examination9. Neurologic examination, with particular attention to

reflexes, vibratory sensation, touch, and proprio-ception

Laboratory EvaluationLaboratory tests should be ordered to establish the

diagnosis of diabetes and to determine the current level ofglycemic control (93). In addition, Phase I laboratory test-ing should provide an evaluation of the patient’s generalmedical condition and should identify associated risk fac-tors. The following laboratory tests should be included inthe Phase I assessment:

1. Fasting or random plasma glucose*2. Glycosylated hemoglobin or fructosamine3. Fasting lipid profile (cholesterol, triglycerides,

HDL/LDL calculation)4. Serum electrolytes*5. Serum creatinine*6. Urinalysis7. Sensitive or ultrasensitive thyroid-stimulating hormone8. Microalbuminuria and creatinine clearance9. Electrocardiography, stress test, or both

*Commonly available as part of a serum chemistryprofile.

Patient Knowledge Base and MotivationThe results of objective testing regarding the physio-

logic aspects and treatment of diabetes mellitus will helpthe clinical endocrinologist or other physician assessthe level of diabetes education to be initiated (94).Psychologic tests and a subjective evaluation of thepatient’s psychologic support systems will help predictpatient adherence to a system of intensive therapy. Theseevaluations will help determine which referrals are mostnecessary and will help establish priorities for educatingthe patient about diabetes self-management.

1. The following evaluation forms may be used toassess the patient’s understanding of the physiolog-ic aspects of diabetes mellitus:a. Diabetes Assessment and Teaching Record (see

Appendix)b. AACE Knowledge Evaluation Forms (see

Appendix)2. The following psychologic tests may be used to

evaluate the patient’s motivation for participating ina diabetes self-management system:a. Michigan Diabetes Research and Training Center

Diabetes Care Profile (Available from MDRTC,University of Michigan Medical Center, G1111Towsley Center, Ann Arbor, MI 48109-0201)

b. Millon Behavioral Health Inventory (Availableto licensed professionals from National Com-puter Systems, PO Box 1294, Minneapolis, MN55440)

3. The patient’s resources and support systems shouldbe evaluated in the following areas, to help assessthe patient’s motivation for adherence to intensivediabetes treatment:a. Familyb. Financial (including medical insurance status)c. Employment

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4. The patient may be reassessed and reevaluated at 6months to determine the level of knowledge retainedafter training and education

Diabetes Self-Management SystemPatient empowerment is vital to a system of intensive

diabetes therapy. For a successful system, the patient mustunderstand and learn to manage the diabetes and its treat-ment (95). Traditional patient education is just one aspectof diabetes intensive self-management. In addition, thepatient with diabetes must be taught to assume responsi-bility for the self-monitoring and problem solving that arecritical to the successful implementation of a system ofintensive diabetes therapy.

Although this educational process is initiated duringPhase I, the information is so vital and the material is soextensive that the educational process should be continuedduring all phases of treatment.

Because each participating patient will have differenteducational needs, the members of the health-care teammust individualize the program. The results of the initialpatient assessment will help health-care team membersestablish a system of priorities for scheduling each topic tobe covered. A series of ongoing patient assessments,undertaken during all subsequent phases of treatment, willhelp health-care team members revise these priorities asneeded to ensure that the individual needs of each patientare being met and to facilitate patient adherence.

Topics to be addressed during the overall course oftreatment of the patient with diabetes may be divided intothe following categories (93):

1. Pathophysiologic features of diabetes2. Rationale for the intensive treatment of diabetes

mellitusa. Potential complications associated with diabetesb. Relationship between control and complications

3. Self-monitoring of blood glucosea. Use of a blood glucose self-monitorb. Schedule for use (minimum of twice daily)c. Instructions for record keeping

4. Medicationa. Descriptionb. Dosing instructionsc. Dosage adjustment algorithmsd. Suggestions for record keeping

5. Nutritiona. Importanceb. Prescribed meal planc. Dealing with nutrition-related fluctuations in

blood glucose levelsd. Suggestions for record keeping

6. Exercisea. Importanceb. Prescribed exercise planc. Dealing with activity-related fluctuations in

blood glucose levelsd. Suggestions for record keeping

7. Recognizing and managing potentially dangerouscomplicationsa. Hypoglycemiab. Diabetic ketoacidosisc. Hypoglycemia unawarenessd. Infectione. Vascular disease

8. Instructions for special situationsa. Sick day rulesb. Travel instructionsc. Use of glucagon

9. Preventive carea. Foot careb. Skin care

10. Psychologic aspectsa. Effect on relationships and family dynamicsb. Effect on self-imagec. Importance of supportd. Denial

11. Instructions for family members

Patient-Physician ContractFor successful implementation of intensive diabetes

management, the patient and the clinical endocrinologistor other physician must have mutual, frequently commu-nicated treatment goals. This relationship necessitates reg-ularly scheduled communication and frequent visitsbetween the patient and members of the health-care team.The frequency of these interactions should be based onindividual patient needs. Patients must be encouraged toadhere to the specified schedule. To achieve this goal, thephysician may need to establish a follow-up system or, insome cases, the intervention of a third-party payer.

For optimal patient adherence to the System ofIntensive Diabetes Self-Management, it may be helpful toelicit the patient’s written commitment to participate. Thedocument, which should be signed by both the patient andthe physician, should specify the responsibilities of bothparties and contain the prescribed schedule of follow-upvisits and communications (see Appendix). The risks ofassuming or declining the responsibility of intensivetherapy need to be defined in the contract.

Phase II: Follow-Up Assessments

A goal of each follow-up assessment is to evaluate thepatient’s physical condition, level of blood glucose con-trol, and degree of adherence to guidelines. Such anassessment should include an interim history, physicalexamination, laboratory evaluation, and review of thepatient’s results of self-monitoring of blood glucose. Onthe basis of the results of this evaluation, the physician andthe patient may elect to revise any or all aspects of thepatient’s treatment plan or the schedule for the assessmentof complications (see Phase III).

Because the patient with diabetes has a considerablyincreased risk of coronary artery and peripheral arterialdisease, dyslipidemia, and hypertension, lipid levels and

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blood pressure must be rigidly monitored and controlled.The patient with diabetes should be viewed comparably toa nondiabetic patient who has had a coronary event. Ashas been substantiated, the reduction of high blood pres-sure in patients with diabetes significantly decreases therisk of nephropathy and retinopathy (55).

Other goals during Phase II are to assess the patient’sunderstanding of diabetes mellitus and the rationale forintensive self-management and to determine the patient’sself-management skills. This evaluation necessitates peri-odic administration of follow-up objective and psycholog-ic tests and inquiry about the patient’s support systems.Depending on the results of this interim assessment, thephysician may reinstitute intensive diabetes education inany deficient areas.

Follow-up assessments should be scheduled at inter-vals of no longer than 3 months and may be combinedwith the modules for assessment of complications (seePhase III).

Interim Patient HistoryThe patient’s responses to the following areas of

questioning should help in the development of a revisedtreatment plan, assessment of existing diabetes-associatedcomplications, and reevaluation of the patient’s risk forfuture complications.

1. Has the patient experienced any acute health prob-lems?

2. Have any changes occurred in any chronic healthproblems?

3. Has the patient experienced any symptoms or signssuggestive of hypoglycemia?

4. Does the patient have any new symptoms or signssuggestive of diabetes-related complications?

5. Have any risk factors changed?

Physical ExaminationPhase II includes an interim physical examination for

each patient. The following elements may be included,depending on patient symptoms and signs and the resultsof the initial physical examination:

1. Height and weight measurements*2. Blood pressure determination, including orthostatic

evaluation*3. Ophthalmoscopic examination4. Thyroid palpation5. Cardiac examination6. Evaluation of pulses, including carotid pulses or

bruit and respiratory variation7. Foot examination*8. Skin examination9. Neurologic examination

*Should be included with every interim physicalexamination.

Every patient should undergo a complete physicalexamination at least once annually.

Laboratory EvaluationDuring each follow-up assessment, the results of the

patient’s self-monitoring of blood glucose should bereviewed. In addition, laboratory tests should be orderedto confirm the patient’s current level of glycemic control.These analyses should include the following:

1. Random plasma glucose2. Glycosylated hemoglobin or fructosamine3. Fasting lipid profile

On the basis of the results of the patient’s self-moni-toring of blood glucose and the laboratory testing, thephysician may elect to revise the recommendationsregarding nutrition, exercise, medication, self-monitoring,and follow-up communication. In addition, the physicianmay elect to revise the schedule for implementing any orall of the Phase III modules for assessment of complica-tions.

Patient Knowledge Base and Self-Management SkillsTo assess the patient’s current level of understanding

of the pathophysiologic features of diabetes mellitus andthe rationale for self-management and to determine thecurrent level of self-management skills, follow-upobjective and psychologic tests should be administered.In addition, the patient’s support systems should be re-evaluated.

1. The following evaluation forms may be used toassess the patient’s current understanding of thephysiologic aspects of diabetes mellitus:a. Diabetes Assessment and Teaching Record (see

Appendix)b. AACE Knowledge Evaluation Forms (see

Appendix)2. The following psychologic test may be used to eval-

uate the patient’s motivation for participating in adiabetes self-management system:a. Michigan Diabetes Research and Training Center

Diabetes Care Profile (Available from MDRTC,University of Michigan Medical Center, G1111Towsley Center, Ann Arbor, MI 48109-0201)

b. Millon Behavioral Health Inventory (Availableto licensed professionals from NationalComputer Systems, PO Box 1294, Minneapolis,MN 55440)

3. The patient’s resources and support systems shouldbe reevaluated in the following areas:a. Familyb. Financial (including medical insurance status)c. Employment

Depending on the results of the interim assessment,the physician may reinstitute intensive education in thedeficient areas or refer the patient to one or more membersof the health-care team.

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Phase III: Assessment of Complications

The goal of Phase III is to assess the presence andseverity of the complications associated with diabetesmellitus. Each of the following four complications mod-ules (93,96) should be performed in conjunction with aquarterly Phase II follow-up assessment:

1. Retinal2. Cardiac-cerebrovascular-peripheral vascular3. Renal4. Neuropathy

Retinal ModuleWhen performed in conjunction with the retinal mod-

ule (96), the Phase II interim history and physical exami-nation should include any questions relevant to the assess-ment of retinal complications. Additional diagnostic eval-uations should include the following:

1. Test of visual acuity (Snellen chart)2. Funduscopic examination3. Intraocular pressure test

In addition to educating the patient about the retinalcomplications that may be associated with diabetes, thephysician should determine—on the basis of the patient’shistory and findings on the current examination—the fre-quency of follow-up and the need for referral to an oph-thalmologist or retinal specialist.

Cardiac-Cerebrovascular-Peripheral Vascular ModuleVascular risk factors should be assessed annually in

adult patients with diabetes. When performed in conjunc-tion with the cardiac-cerebrovascular-peripheral vascularmodule (93), the Phase II interim history and physicalexamination should include any questions relevant to theassessment of cardiac-cerebrovascular-peripheral vascularcomplications. Additional diagnostic evaluations shouldinclude the following:

1. Electrocardiography and rhythm strip, stress test, orboth (based on the patient’s age and symptoms)

2. Lipid profile (cholesterol, triglycerides, HDL/LDLcalculation)

3. Evaluation of peripheral pulses by physical or objec-tive testing (or both)

In addition to educating the patient about the vascularcomplications that may be associated with diabetes, thephysician should determine—on the basis of the patient’shistory and findings on the current examination—the fre-quency of follow-up, the need for more intensive cardiactesting, and the need for referral to a cardiologist, neurol-ogist, interventional radiologist, or vascular surgeon.

Renal ModuleWhen performed in conjunction with the renal mod-

ule (93), the Phase II interim history and physical exami-

nation should include any questions relevant to the assess-ment of renal complications. Additional diagnostic evalu-ations should include the following:

1. Test for microalbuminuria2. Creatinine clearance3. Automated serum chemistry analysis

In addition to educating the patient about the renalcomplications that may be associated with diabetes, thephysician should determine—on the basis of the patient’shistory and findings on the current examination—thefrequency of follow-up and the need for referral to anephrologist.

Neuropathy ModuleWhen performed in conjunction with the neuropathy

module (93), the Phase II interim history and physicalexamination should include any questions relevant to theassessment of neuropathy. Additional diagnostic evalua-tions should include the following:

1. A review of symptoms relevant to peripheral nerveand autonomic dysfunction

2. Module-specific testing (vibratory sensation, soft-touch, pinprick, evaluation of autonomic dysfunc-tion—for example, R-R interval variation withpaced breathing)

In addition to educating the patient about neuropathy,the physician should determine—on the basis of thepatient’s history and findings on the current examina-tion—the frequency of follow-up and the need for referralto a neurologist.

CONCLUSION

AACE has provided the recent scientific evidence thatcontinues to support its Medical Guidelines for theManagement of Diabetes Mellitus: A System of IntensiveDiabetes Self-Management. A thriving patient-physicianrelationship and a partnership effort among the patient, thephysician, and the diabetes management team remain crit-ical to the success of intensive diabetes self-management.These coordinated efforts should result in normalization ornear-normalization of the patient’s glycosylated hemoglo-bin value and blood glucose level. The outcome will be anenhancement in the patient’s quality of life, a decrease inmorbidity, and a reduction in mortality.

The patient must be committed to learning diabetesself-management, and the physician and the diabetes self-management team must be dedicated to teaching thepatient the appropriate techniques and the rationale forthem. AACE hopes that the use of these guidelines byphysicians and patients will lead to improved care forpatients with diabetes, an augmented quality of life forsuch patients, and decreased overall costs of diabetes carefor the individual patients and society.

62 AACE Diabetes Guidelines, Endocr Pract. 2002;8(Suppl 1)

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37. Wasserman DH, Spalding JA, Lacy DB, Colburn CA,Goldstein RE, Cherrington AD. Glucagon is a primarycontroller of hepatic glycogenolysis and gluconeogenesisduring muscular work. Am J Physiol. 1989;257(1 Pt1):E108-E117.

38. Sato Y, Iguchi A, Sakamoto N. Biochemical determina-tion of training effects using insulin clamp technique.Horm Metab Res. 1984;16:483-486.

39. Devlin JT, Hirshman M, Horton ED, Horton ES.Enhanced peripheral and splanchnic insulin sensitivity inNIDDM men after single bout of exercise. Diabetes.1987;39:434-439.

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41. Physicians’ Desk Reference. 53rd ed. Montvale, NJ:Medical Economics Company, 1999.

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primary-prevention trial with gemfibrozil in middle-agedmen with dyslipidemia; safety of treatment, changes inrisk factors, and incidence of coronary heart disease. NEngl J Med. 1987;317:1237-1245.

50. Pyorala K, Pedersen TR, Kjekshus J, Faergeman O,Olsson AG, Thorgeirsson G. Cholesterol lowering withsimvastatin improves prognosis of diabetic patients withcoronary heart disease: a subgroup analysis of theScandinavian Simvastatin Survival Study (4S) [publishederratum appears in Diabetes Care. 1 9 9 7 ; 2 0 : 1 0 4 8 ] .Diabetes Care. 1997;20:614-620.

51. Sacks FM, Pfeffer MA, Moye LA, et al. (Cholesteroland Recurrent Events Trial Investigators). The effectof pravastatin on coronary events after myocardial infarc-tion in patients with average cholesterol levels. N Engl JMed. 1996;335:1001-1009.

52. Downs JR, Clearfield M, Weis S, et al. Primary preven-tion of acute coronary events with lovastatin in men andwomen with average cholesterol levels: results ofAFCAPS/TexCAPS; Air Force/Texas Coronary Athero-sclerosis Prevention Study. JAMA. 1998;279:1615-1622.

53. O’Brien T, Nguyen TT, Zimmerman BR. Hyperlip-idemia and diabetes mellitus. Mayo Clin Proc. 1998;73:969-976.

54. Austin MA, Hokanson JE, Edwards KL. Hypertrigly-ceridemia as a cardiovascular risk factor. Am J Cardiol.1998;81:7B-12B.

55. UK Prospective Diabetes Study Group. Tight bloodpressure control and risk of macrovascular and microvas-cular complications in type 2 diabetes: UKPDS 38 [pub-lished erratum appears in BMJ. 1999;318:29]. BMJ. 1998;317:703-713.

56. Lewis EJ, Hunsicker LG, Bain RP, Rohde RD, TheCollaborative Study Group. The effect of angiotensin-converting-enzyme inhibition on diabetic nephropathy

[published erratum appears in N Engl J Med. 1993;330:152]. N Engl J Med. 1993;329:1456-1462.

57. Ravid M, Savin H, Jutrin I, Bental T, Katz B, LishnerM. Long-term stabilizing effect of angiotensin-convertingenzyme inhibition on plasma creatinine and on proteinuriain normotensive type II diabetic patients. Ann Intern Med.1993;118:577-581.

58. O’Driscoll G, Green D, Maiorana A, Stanton K,Colreavy F, Taylor R. Improvement in endothelial func-tion by angiotensin-converting enzyme inhibition in non-insulin-dependent diabetes mellitus. J Am Coll Cardiol.1999;33:1506-1511.

59. Black HR, Cohen JD, Kaplan NM, et al. The sixthreport of the Joint National Committee on Prevention,Detection, Evaluation, and Treatment of High BloodPressure. Arch Intern Med. 1997;157:2413-2445.

60. Colwell JA. Aspirin therapy in diabetes. Diabetes Care.1997;20:1767-1771.

61. Alfthan G, Aro A, Gey KF. Plasma homocysteine andcardiovascular disease mortality [letter]. Lancet. 1997;349:397.

62. Bloomgarden ZT. International Diabetes FederationMeeting, 1997, and other recent meetings: atherosclerosisand related topics. Diabetes Care. 1998;21:1356-1363.

63. Malmberg K, Norhammar A, Wedel H, Ryden L.Glycometabolic state at admission: important risk markerof mortality in conventionally treated patients with dia-betes mellitus and acute myocardial infarction; long-termresults from the Diabetes and Insulin-Glucose Infusion inAcute Myocardial Infarction (DIGAMI) Study.Circulation. 1999;99:2626-2632.

64. Hellman R. A new approach in intensive therapy for type2 diabetes. Practical Diabetology. 1998;17:21-26.

65. Janand-Delenne B, Savin B, Habib G, Bory M, VagueP, Lassmann-Vague V. Silent myocardial ischemia inpatients with diabetes: who to screen. Diabetes Care.1999;22:1396-1400.

66. Nesto RW. Screening for asymptomatic coronary arterydisease in diabetes. Diabetes Care. 1999;22:1393-1395.

67. Herman WH, Dasbach EJ, Songer TJ, Eastman RC.The cost-effectiveness of intensive therapy for diabetesmellitus. Endocrinol Metab Clin North Am. 1997;26:679-695.

68. American Diabetes Association. Economic conse-quences of diabetes mellitus in the U.S. in 1997. DiabetesCare. 1998;21:296-309.

69. Rubin RJ, Altman WM, Mendelson DN. Health careexpenditures for people with diabetes mellitus, 1992. JClin Endocrinol Metab. 1994;78:809A-809F.

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71. Eastman R, Fleming B, Vinocor F, Pogash L. Cost andconsequences of ADA treatment targets [abstract 0136].Program and abstracts of the American DiabetesAssociation Annual Meeting, 1997, page 35A.

72. Gilmer TP, O’Connor PJ, Manning WG, Rush WA.The cost to health plans of poor glycemic control.Diabetes Care. 1997;20:1847-1853.

73. Diabetes Control and Complications Trial ResearchGroup. Resource utilization and costs of care in theDiabetes Control and Complications Trial. Diabetes Care.1995;18:1468-1478.

74. Cobin RH. Endocrinologists provide cost effective dia-betes care. First Messenger. 1997;6(No. 5):8-10.

75. Diabetes Control and Complications Trial ResearchGroup. Lifetime benefits and costs of intensive therapy aspracticed in the Diabetes Control and Complications Trial

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76. Testa MA, Simonson DC. Health economic benefits andquality of life during improved glycemic control inpatients with type 2 diabetes mellitus: a randomized, con-trolled, double-blind trial. JAMA. 1998;280:1490-1496.

77. May ME, Young C, King J. Resource utilization in treat-ment of diabetic ketoacidosis in adults. Am J Med Sci.1993;306:287-294.

78. Alsever RN. Specialist versus primary care: not an easyquestion. Physician Exec. 1995;21:39-41.

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80. Levetan CS, Passaro MD, Jablonski KA, Ratner RE.Effect of physician specialty on outcomes in diabeticketoacidosis. Diabetes Care. 1999;22:1790-1795.

81. Reaven GM. Insulin resistance and its consequences:non-insulin-dependent diabetes mellitus and coronaryheart disease. In: LeRoith D, Taylor SI, Olefsky JM, eds.Diabetes Mellitus. Philadelphia: Lippincott-RavenPublishers, 1996: 509-519.

82. American Diabetes Association. C o n s e n s u sDevelopment Conference on Insulin Resistance. 5-6November 1997. Diabetes Care. 1998;21:310-314.

83. Despres JP, Lamarche B, Mauriege P, et al.Hyperinsulinemia as an independent risk factor forischemic heart disease. N Engl J Med. 1996;334:952-957.

84. Chen Y-DI, Reaven GM. Insulin resistance and athero-sclerosis. Diabetes Rev. 1997;5:331-342.

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86. Hsueh WA, Quinones MJ, Creager MA. Endotheliumin insulin resistance and diabetes. Diabetes Rev.1997;5:343-352.

87. Polonsky KS, Sturis J, Bell GI. Seminars in Medicine ofthe Beth Israel Hospital, Boston: non-insulin-dependentdiabetes mellitus—a genetically programmed failure ofthe beta cell to compensate for insulin resistance. N EnglJ Med. 1996;334:777-783.

88. Benson EA, Holdaway IM. Insulin receptors in humancancer. Br J Cancer. 1981;44:917-920.

89. Dunaif A, Scott D, Finegood D, Quintana B, WhitcombR. The insulin-sensitizing agent troglitazone improvesmetabolic and reproductive abnormalities in the polycys-tic ovary syndrome. J Clin Endocrinol Metab. 1996;81:3299-3306.

90. Kissebah AH. Central obesity: measurement and meta-bolic effects. Diabetes Rev. 1997;5:8-20.

91. Ruderman N, Chisholm D, Pi-Sunyer X, Schneider S.The metabolically obese, normal-weight individual revis-ited. Diabetes. 1998;47:699-713.

92. Helmrich SP, Ragland DR, Leung RW, PaffenbargerRS Jr. Physical activity and reduced occurrence of non-insulin-dependent diabetes mellitus. N Engl J Med.1991;325:147-152.

93. American Diabetes Association. Standards of medicalcare for patients with diabetes mellitus [position state-ment]. Diabetes Care. 1991;14:10-13.

94. Davidson MB. Diabetes Mellitus: Diagnosis andTreatment. 3rd ed. New York: Churchill Livingstone,1991: 330.

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AACE Diabetes Guidelines, Endocr Pract. 2002;8(Suppl 1) 65

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AACE Diabetes Guidelines, Endocr Pract. 2002;8(Suppl 1) 67III. Educational Objectives/Plan

Date Objectives Met

1.

2.

3.

IVa. Nutrition Histor y

Time:

Breakfast:

Snack:

Lunch:

Snack:

Dinner:

Snack:

Food preferences/intolerances:

IVb. Meal Plan Prescribed Total Daily Caloric Intake:

Milk Veg Fruit Starch Lean Meat Fat

Breakfast:

Midmorning Snack:

Lunch:

Afternoon Snack:

Dinner:

Bedtime Snack:

V. Previous Diabetes EducationDate Place

Will anyone else attend the education sessions? Yes No Name

Frequency of:

DKA Low BS High BS Diabetic Hospitalizations

Complications:

Retinopathy I BP Nephropathy Neuropathy PVD Other

Smoke Amount Drink Alcohol Amount Type

Exercise:

Type Times/Week How Long

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68 AACE Diabetes Guidelines, Endocr Pract. 2002;8(Suppl 1)

VI. Teaching Record

A. Basic Pathophysiology

Understands the basic pathophysiology of diabetes

B. Psychologic Adjustment

Has psychologically adjusted to diabetes

and lifestyle modifications and understands

effects of stress on management

C. Family Involvement

Family and/or significant other(s) are sufficiently

involved in diabetes management

S M W D

D. Exercise

Describes, unders tands, and incorporates effective

exercise habits into diabetes management

E. Medications

Demonstrates and/or verbalizes correct use of

1. P.O. Type

D o s a g e

F r e q u e n c y

A c t i o n

2. Insulin

T y p e / D o s e

A c t i o n

Injection Techniques

M i x i n g

S t o r a g e

Site Selection

F. Relationship Among

Nutrition/Exercise/Medication

Understands interrelation of nutrition, exercise,

medication, and lab values and

incorporates th is into diabetes management

G. Monitoring

1 . Demonstrates accurate blood or ur ine

glucose monitoring

2 . F r e q u e n c y

3 . T y p e

4 . Urine ketone testing

H. Hypoglycemia

Understands, describes, and appropriate ly reacts to

and treats the signs and symptoms of hypoglycemia

I. Illness/Hyperglycemia

Understands, describes, and appropriately responds

to the signs and symptoms of illness and/or

hyperglycemia; ketones

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AACE Diabetes Guidelines, Endocr Pract. 2002;8(Suppl 1) 69

VI. Teaching Record ( c o n t i n u e d )

J. Complications (Prevent, Treat, Rehabilitate)

Understands the complicat ions of diabetes and

practices health-care measures to manage and assist

in rehabilitation of those complications:

N e u r o p a t h y

N e p h r o p a t h y

R e t i n o p a t h y

I m p o t e n c e

BP Control

K. Care Benefits/Responsibilities

Understands the benefits and responsibili ties

of appropriate diabetes management

L. Hygiene

Understands the importance of and practices routine

hygiene to prevent possible diabetes complicat ions

Foot care

Eye care

Dental Care

G e n e r a l

M. Use of Health-Care Systems

Is aware of and appropriately uses health-care systems

(financia l resources, health insurance) and knows how

to reach health-care team and emergency care

N. Community Resources

Is aware of and appropriately uses available community

resources (ADA, MedicAlert®, support groups)

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70 AACE Diabetes Guidelines, Endocr Pract. 2002;8(Suppl 1)

VIIb. Follow-up/Continuing Education

A. Demonstrates how to plan appropriate meals

from the meal plan

B. States the caloric level of the meal plan

and the percentages of carbohydrate,

protein, and fat

C. Lists food sources of dietary fiber

and describes how to incorporate foods

with fiber into the meal plan

D. Demonstrates how to select foods

in appropriate portion sizes

E. Demonstrates how to select appropriate

foods when dining out

F. States the need to be consistent

in daily caloric intake

G. States the benefi ts of making permanent

li festyle changes in nutr ition and

activity levels

Other:

VIII. Evaluation Summary/Follow-up

Pretest Score: Date:

Posttest Score: Date:

Signatures

RN, CDE

RD/LD

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AACE Knowledge Evaluation Forms

The AACE Knowledge Evaluation Forms are to beused to assess the patient’s knowledge of diabetes beforeand after exposure to the system of intensive diabetesmanagement in order to detect weaknesses in the patient’sunderstanding and provide appropriate useful information.The educational process need not begin with basic ele-ments in an already knowledgeable patient. The goals areto provide the information needed for self-management ofdiabetes and to encourage adherence.

Sample forms without the answers starred are avail-able from the AACE office on request and may be photo-copied.

Type 2 Diabetes: Patient Evaluation

What Is Diabetes?

1. In type 2 diabetes, the bodya. cannot use insulin well*b. makes no insulin at allc. rejects insulind. destroys insulin

2. Patients with type 2 diabetesa. never need insulin injectionsb. need insulin injections dailyc. may need insulin injections*

3. Insulin is made in thea. liverb. stomachc. kidneysd. pancreas*

4. Insulin helps the bodya. turn sugar into energy*b. get rid of sugarc. store sugar in the bloodd. make red blood cells

5. “Blood glucose” refers to the level of sugar (glu-cose) in the blood.a. true*b. false

6. The target range for blood glucose before meals isa. 50 to 70 mg/dLb. 70 to 120 mg/dL*c. 125 to 160 mg/dLd. 160 to 200 mg/dL

7. “Hyperglycemia” meansa. high blood glucose*b. low blood glucose

c. high blood pressured. low blood pressure

8. “Hypoglycemia” meansa. high blood pressureb. low blood pressurec. high blood glucosed. low blood glucose*

9. Which of the following is a symptom of hypo-glycemia?a. weaknessb. sweatingc. shakinessd. all of the above*

10. The aim of intensive diabetes treatment isa. to keep blood glucose as close to normal as

possibleb. to avoid long-term complicationsc. both of the above*

11. Complications of diabetes includea. kidney diseaseb. eye problemsc. foot problemsd. all of the above*

12. Which of the following can affect blood glucosecontrol?a. stressb. eating habitsc. exercised. all of the above*

13. Patients with diabetes have no control over thedevelopment of complications.a. trueb. false*

14. “Tight” control of diabetes meansa. keeping blood glucose as close to normal as

possibleb. frequent self-monitoringc. reduced complicationsd. all of the above*

15. Treatment of type 2 diabetes is usually initiated witha. insulinb. diet and exercise programs*c. diabetes pills

16. The most important person on your health-care teamisa. you*b. the doctorc. the diabetes educatord. the dietitian

AACE Diabetes Guidelines, Endocr Pract. 2002;8(Suppl 1) 71

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Nutrition

1. In overweight patients with diabetes, losing weightmaya. help the body use insulin betterb. lower blood glucosec. decrease the risk of heart diseased. do all of the above*

2. Meals should generally be eatena. 1 to 2 hours apartb. 4 to 5 hours apart*c. every 6 hoursd. whenever you want

3. Carbohydrates should make up what percent of yourdaily calories?a. 5 to 10%b. 15%c. 25%d. 55 to 60%*

4. A good source of complex carbohydrates isa. eggsb. mayonnaisec. whole-grain bread*d. roast beef

5. Fat should constitute what percent of your dailycalories?a. less than 30%*b. 45%c. 55 to 60%d. 75%

6. Which of the following foods is high in fat?a. applesb. lettucec. cheddar cheese*d. oatmeal

7. The fatty substance in food linked to heart disease isa. carbohydratesb. proteinc. cholesterol*d. fiber

8. To decrease dietary fat and cholesterol, which foodis the best choice?a. steakb. fried eggsc. broiled chicken without skin*d. ham and cheese sandwich

9. How much cholesterol should you have a day?a. 1,200 mgb. 750 mgc. 500 mgd. no more than 300 mg*

10. Which of the following foods contain cholesterol?a. eggsb. Swiss cheesec. red meatd. all of the above*

11. How much of your diet should be protein?a. less than 10%b. 15 to 20%*c. 50%d. 75%

12. Which of the following foods provides low-fatprotein?a. broiled flounder*b. Swiss cheesec. carrotsd. saltines

13. The maximum daily amount of salt (sodium) in yourdiet should bea. less than 3 g*b. 5 gc. 10 gd. 12 g

14. One serving of alcohol equalsa. 12 ounces of beerb. 2 ounces of winec. 1.5 ounces of scotchd. all of the above*

15. If alcohol is allowed, you should drink ita. on an empty stomachb. along with food*

16. If alcohol is allowed, which is not a good choice?a. dry white wineb. sweet liqueur*c. scotch and waterd. beer

17. A “free food”a. has no sugarb. has fewer than 20 calories*c. has no saltd. can be eaten in unlimited quantities

18. Patients with diabetes should never eat inrestaurants.a. trueb. false*

19. Which of the following may help lower bloodglucose?a. fatb. proteinc. soluble fiber*d. all of the above

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20. Which food provides soluble fiber?a. lentilsb. oatsc. fruitsd. all of the above*

21. Which of the following should not be used bypatients with diabetes?a. aspartameb. honey*c. saccharind. fructose

22. People with diabetes need more vitamins and miner-als than do people without diabetes.a. trueb. false*

23. The number of calories eaten should bea. greatest at breakfastb. greatest at lunchc. greatest at dinnerd. evenly distributed among meals*

24. All patients with diabetes follow the same mealplan.a. trueb. false*

25. “Exchange” refers to foods thata. can be substituted for each other*b. must be returned because they contain sugarc. can be shared with friendsd. must be avoided

Exercise

1. Regular exercisea. improves lipid levelsb. strengthens the heartc. gives a sense of well-beingd. does all of the above*

2. Regular exercise maya. lower blood glucoseb. reduce the amount of insulin neededc. reduce the amount of diabetes pills neededd. do all of the above*

3. Which exercise is best for patients with “insensi-tive” feet?a. swimming*b. joggingc. runningd. tap dancing

4. In general, fit patients with diabetes should exercisefora. 15 minutes once a weekb. 1 hour once a weekc. 20 to 30 minutes 3 times a week*d. 1 hour every day

5. Patients who need insulin should inject it into thethigh muscle before running.a. trueb. false*

6. If blood glucose is less than 80 mg/dL during exer-cise, you shoulda. lie downb. eat a snack*c. call your doctor immediatelyd. ignore it and keep exercising

7. If blood glucose is more than 300 mg/dL, insulinshould be adjusted or exercise should be delayed.a. true*b. false

8. For avoidance of hypoglycemia, the best time toexercise isa. any time you are hungryb. just before dinnerc. after meals*d. just before breakfast

Monitoring

1. Low blood glucose can be detected accurately bytestinga. urineb. blood*c. salivad. all of the above

2. Self-monitoring of blood glucose isa. essential for intensive therapyb. the key to determining the right amount of med-

icationc. useful even if diabetes is controlled with diet

and exercised. all of the above*

3. With intensive therapy, self-monitoring of bloodglucose should be donea. only before breakfastb. only before lunchc. only before dinnerd. several times a day*

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4. Monitoring should be done more oftena. on sick daysb. when travelingc. when meal or exercise plans changed. at all of the above times*

5. Patients with diabetes should undergo assessment bytheir clinical endocrinologist or another physiciana. every 3 months*b. every yearc. every 2 yearsd. only after complications develop

6. A glycosylated hemoglobin test measures blood glu-cose over the pasta. hourb. dayc. weekd. 8 to 12 weeks*

7. In people without diabetes, the normal glycosylatedhemoglobin value is abouta. 8 to 10%b. 3.8 to 6.0%*c. 2.5 to 3.5%d. 10.1 to 11.8%

8. During illness, blood glucose should be monitoredeverya. 1/2 hourb. 3 to 4 hours*c. 6 hoursd. 12 hours

9. To treat mild hypoglycemia, you coulda. take 3 glucose tabletsb. eat a few pieces of candy (not sugar-free)c. eat 2 tablespoons of raisinsd. do any of the above*

10. Nighttime hypoglycemia should be treated witha. carbohydrateb. proteinc. fatd. first carbohydrate, then carbohydrate plus pro-

tein*

Medications

1. Diabetes pillsa. lower blood glucoseb. increase the release of insulinc. fight insulin resistanced. do all of the above*

2. For diabetes pills to work, the body must be able tomake some insulin.a. true*b. false

3. Sources of insulin used for injections area. pigsb. cowsc. synthesis by recombinant DNAd. all of the above*

4. The insulin you are using should be stored ina. the refrigeratorb. the freezerc. the medicine cabinetd. a cool, dry place*

5. The preferred site for an insulin injection isa. the abdomen*b. the hipsc. the buttocksd. all of the above

6. Insulin should always be injected in the same site.a. trueb. false*

7. When you travel, your medications and suppliesshould bea. checked in your luggageb. carried with you*c. left at home

8. During illness, you should stop taking your medica-tions.a. trueb. false*

Type 1 Diabetes: Patient Evaluation

What Is Diabetes?

1. In type 1 diabetes mellitus, the body does not makeenougha. salivab. insulin*c. glucosed. cholesterol

2. Patients with type 1 diabetesa. never need insulin injectionsb. need insulin injections daily*c. may occasionally need insulin injections

3. Insulin is made in thea. liverb. stomachc. kidneysd. pancreas*

4. Insulin helps the bodya. turn sugar into energy*b. get rid of sugarc. store sugar in the bloodd. make red blood cells

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5. “Blood glucose” refers to the level of sugar(glucose) in the blood.a. true*b. false

6. The target range for blood glucose before meals isa. 50 to 70 mg/dLb. 70 to 120 mg/dL*c. 125 to 160 mg/dLd. 160 to 200 mg/dL

7. “Hyperglycemia” meansa. high blood glucose*b. low blood glucosec. high blood pressured. low blood pressure

8. “Hypoglycemia” meansa. high blood pressureb. low blood pressurec. high blood glucosed. low blood glucose*

9. Which of the following is a symptom of hypo-glycemia?a. weaknessb. sweatingc. shakinessd. all of the above*

10. The aim of intensive diabetes treatment isa. to keep blood glucose as close to normal as

possibleb. to avoid long-term complicationsc. both of the above*

11. Complications of diabetes includea. kidney diseaseb. eye problemsc. foot problemsd. all of the above*

12. Which of the following can affect blood glucosecontrol?a. stressb. eating habitsc. exercised. all of the above*

13. Patients with diabetes have no control over thedevelopment of complications.a. trueb. false*

14. “Tight” control of diabetes meansa. keeping blood glucose as close to normal as

possibleb. frequent self-monitoringc. reduced complicationsd. all of the above*

15. The most important person on your health-care teamisa. you*b. the doctorc. the diabetes educatord. the dietitian

Nutrition

1. Carbohydrates should make up what percent of yourdaily calories?a. 5 to 10%b. 15%c. 25%d. 55 to 60%*

2. A good source of complex carbohydrates isa. eggsb. mayonnaisec. whole-grain bread*d. roast beef

3. Fat should constitute what percent of your dailycalories?a. less than 30%*b. 45%c. 55 to 60%d. 75%

4. Which of the following foods is high in fat?a. applesb. lettucec. cheddar cheese*d. oatmeal

5. The fatty substance in food linked to heart disease isa. carbohydratesb. proteinc. cholesterol*d. fiber

6. Which of the following foods contain cholesterol?a. eggsb. Swiss cheesec. red meatd. all of the above*

7. To decrease dietary fat and cholesterol, which foodis the best choice?a. steakb. fried eggsc. broiled chicken without skin*d. ham and cheese sandwich

8. How much of your diet should be protein?a. less than 10%b. 15 to 20%*c. 50%d. 75%

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9. Which of the following foods provides low-fatprotein?a. broiled flounder*b. Swiss cheesec. carrotsd. saltines

10. The maximum daily amount of salt (sodium) in yourdiet should bea. less than 3 g*b. 5 gc. 10 gd. 12 g

11. One serving of alcohol equalsa. 12 ounces of beerb. 2 ounces of winec. 1.5 ounces of scotchd. all of the above*

12. If alcohol is allowed, you should drink ita. on an empty stomachb. along with food*

13. If alcohol is allowed, which is not a good choice?a. dry white wineb. sweet liqueur*c. scotch and waterd. beer

14. A “free food”a. has no sugarb. has fewer than 20 calories*c. has no saltd. can be eaten in unlimited quantities

15. Which one of the following should not be used bypatients with diabetes?a. aspartameb. honey*c. saccharind. fructose

16. “Exchange” refers to foods thata. can be substituted for each other*b. must be returned because they contain sugarc. can be shared with friendsd. must be avoided

Exercise

1. Regular exercisea. improves lipid levelsb. strengthens the heartc. gives a sense of well-beingd. does all of the above*

2. Which exercise is best for patients with “insensi-tive” feet?a. swimming*b. joggingc. runningd. tap dancing

3. In general, fit patients with diabetes should exercisefora. 15 minutes once a weekb. 1 hour once a weekc. 20 to 30 minutes 3 times a week*d. 1 hour every day

4. Patients who need insulin should inject it into thethigh muscle before running.a. trueb. false*

5. If blood glucose is less than 80 mg/dL duringexercise, you shoulda. lie downb. eat a snack*c. call your doctor immediatelyd. ignore it and keep exercising

6. If blood glucose is more than 300 mg/dL, insulinshould be adjusted or exercise should be delayed.a. true*b. false

7. For avoidance of hypoglycemia, the best time toexercise isa. any time you are hungryb. just before dinnerc. after meals*d. just before breakfast

Monitoring

1. Low blood glucose can be detected accurately bytestinga. urineb. blood*c. salivad. all of the above

2. Self-monitoring of blood glucose isa. essential for intensive therapyb. the key to determining the right amount of med-

icationc. important to see the effect of food intaked. all of the above*

3. With intensive therapy, self-monitoring of bloodglucose should be donea. only before breakfastb. only before lunchc. only before dinnerd. several times a day*

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4. Monitoring should be done more oftena. on sick daysb. when travelingc. when meal or exercise plans changed. at all of the above times*

5. If your blood glucose is more than 240 mg/dL andyour urine contains large ketones, you shoulda. take a napb. take extra insulin, then call your doctor*c. eat a large meald. exercise

6. Ketoacidosis may be caused bya. very high blood glucoseb. very little insulin*c. too much insulind. too much food

7. Patients with diabetes should undergo assessment bytheir clinical endocrinologist or another physiciana. every 2 yearsb. every 5 yearsc. every 3 months*d. only after complications develop

8. A glycosylated hemoglobin test measures blood glu-cose over the pasta. hourb. dayc. weekd. 8 to 12 weeks*

9. In people without diabetes, the normal glycosylatedhemoglobin value is abouta. 8 to 10%b. 3.8 to 6.0%*c. 2.5 to 3.5%d. 10.1 to 11.8%

10. During illness, blood glucose should be monitoredeverya. 1/2 hourb. 3 to 4 hours*c. 6 hoursd. 12 hours

11. To treat mild hypoglycemia, you coulda. take 3 glucose tabletsb. eat a few pieces of candy (not sugar-free)c. eat 2 tablespoons of raisinsd. do any of the above*

12. Nighttime hypoglycemia should be treated witha. carbohydrateb. proteinc. fatd. first carbohydrate, then carbohydrate plus pro-

tein*

Medications1. Sources of insulin used for injections are

a. pigsb. cowsc. synthesis by recombinant DNAd. all of the above*

2. The insulin you are using should be stored ina. the refrigeratorb. the freezerc. the medicine cabinetd. a cool, dry place*

3. The best site for an insulin injection isa. the abdomen*b. the hipsc. the buttocksd. all of the above

4. Insulin should always be injected in the same site.a. trueb. false*

5. When you travel, your medications and suppliesshould bea. checked in your luggageb. carried with you*c. left at home

6. During illness, you should stop taking your medica-tions.a. trueb. false*

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78 AACE Diabetes Guidelines, Endocr Pract. 2002;8(Suppl 1)

Sample Patient-Physician Contract

I understand that if I agree to participate in the System of Intensive Diabetes Self-Management, I will be expected to dothe following:

1. Dedicate myself to getting my blood glucose level as close to normal as possible by following the instructions of thediabetes self-management team

2. Regularly visit the clinic for a physical examination, laboratory tests, and nutrition counseling; follow-up visits willbe scheduled every 3 months or more frequently if deemed necessary by my physician or other members of myhealth-care team

3. Bring a detailed 1-day food record to each follow-up visit, provide necessary nutrition information for me and mydietitian, and adjust my eating habits to meet the nutrition goals established by my dietitian

4. Use medications as prescribed by my health-care team

5. Monitor my blood glucose levels at home as instructed and bring the results to each follow-up visit

6. Follow my prescribed exercise plan

7. Obtain identification as a patient with diabetes, for prompt assistance in case of an emergency

8. Ask my physician and other members of my health-care team to explain any aspect of my care that I do not entirelyunderstand

I understand that if I do not monitor myself carefully, there is a risk of hypoglycemia.

I also understand that if I do not strive to normalize my blood glucose, I am at increased risk of developing thecomplications of diabetes mellitus.

My signature indicates that I have read and understand the above agreement.

__________________________________________Patient

________________Date

I agree to provide the leadership for the diabetes self-management team. Team members will be available to answeryour questions and help you self-manage your diabetes. I will continue to encourage you to maintain the best possiblecontrol of your diabetes.

__________________________________________Physician

________________Date

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AACE Diabetes Guidelines, Endocr Pract. 2002;8(Suppl 1) 79

Schedule:Phase I: Initial Assessment Multiple visits over 3-4 weeks

Goals Diagnostic tools Action steps

Assess patient’s disease Complex history Develop recommendations for

status and risk factors •Medical (including chief complaint, •Nutrition

duration of known disease) •Exercise

•Family, personal •Medication

•Gestational •Blood glucose self-monitoring

•Weight, nutrition •Record keeping

•Exercise

•Treatment Schedule appropriate modular

•Symptoms of complications evaluation and referrals for

•Risk factors complications or risk factor

modification

Complex physical examination to be

done by clinical endocrinologist or

other physician

•Height, weight

•Blood pressure (including orthostatic)

•Ophthalmoscopy

•Thyroid palpation

•Cardiac assessment

•Pulses

•Feet

•Skin

•Neurologic system

Complex laboratory tests to be done

and evaluated by clinical

endocrinologist or other physician

•Fasting or random plasma glucose

•Glycosylated hemoglobin

•Fasting lipid profile

•Serum electrolytes

•Serum creatinine

•Urinalysis

•Thyrotropin

•Microalbuminuria

•Creatinine clearance

•Electrocardiography, stress test

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80 AACE Diabetes Guidelines, Endocr Pract. 2002;8(Suppl 1)

Phase I: Initial Assessment (continued)

Goals Diagnostic tools Action steps

Assess patient’s knowledge Objective tests Initiate discussion of diabetes self-

base and motivation to learn •Diabetes Assessment and management topics

Teaching Record

Initiate appropriate level of •AACE Knowledge Evaluation Refer to

diabetes education Forms •Diabetes educator (1-2 hours ASAP)

•Dietitian (1-2 hours ASAP)

Psychologic tests •Exercise physiologist, if necessary

•Michigan Diabetes Research and •Psychologist, if necessary

Training Center Diabetes Care

Profile

•Millon Behavioral Health

Inventory

Support systems evaluation

•Family

•Financial

•Employment

Obtain patient agreement Patient-physician contract Explain

to intensive diabetes •Pathophysiologic features of diabetes

treatment and initiate •Rationale for intensive treatment

diabetes self-management •Patient role in diabetes self-

management

Provide instructions regarding

•Blood glucose self-monitoring

•Medication (including dosage-

adjustment algorithms)

•Nutrition

•Exercise

•Complications

•Special situations

•Preventive care

•Psychologic aspects

Review schedule of follow-up

communications (telephone, office

visits) among patient, clinical

endocrinologist, and health-care

team

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AACE Diabetes Guidelines, Endocr Pract. 2002;8(Suppl 1) 81

Schedule:3-month intervals

Phase II: Follow-Up Assessments (in combination with complications modules)

Goals Diagnostic tools Action steps

Evaluate blood glucose control Interim history Revise recommendations for

and disease complications •Acute problems •Nutrition

•Chronic problems •Exercise

•Hypoglycemia •Medication (including dosage-

•New symptoms suggestive adjustment algorithms)

of complications •Blood glucose self-monitoring

•Change in risk factors •Follow-up communications between

patient and health-care team

Laboratory tests

•Random plasma glucose Make any necessary

•Glycosylated hemoglobin adjustments to scheduling of

•Lipids, if necessary complications modules

Results of blood glucose (see Phase III)

self-monitoring

Physical examination

•Height, weight

•Blood pressure (including

orthostatic)

•Ophthalmoscopy

•Thyroid palpation

•Cardiac assessment

•Pulses

•Feet

•Skin

•Neurologic system

6-month visit

Evaluate patient’s understanding Objective tests Initiate intensive education in areas

of diabetes mellitus and Psychologic tests of deficiency, if necessary

rationale for self-management

Support systems reevaluation Refer (as needed) to

•Diabetes educator

Assess patient’s self- •Dietitian

management skills •Exercise physiologist

•Psychologist

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82 AACE Diabetes Guidelines, Endocr Pract. 2002;8(Suppl 1)

Schedule:Each module to be performed annually

Phase III: Assessment of Complications Initiate at 9-month visit

Goals Diagnostic tools Action steps

Retinal module Module-specific follow-up Educate patient about retinalassessment, including complicationsophthalmoscopy

Determine frequency of follow-Test of visual acuity (Snellen up—on the basis of presence or

chart) absence of complications

Funduscopic examination and Refer to ophthalmologist—on thephotographs (if indicated) basis of age, duration of disease, and

findings on current examinationIntraocular pressure test

Cardiac-cerebrovascular- Module-specific follow-up Educate patient about vascularperipheral vascular assessment, including pulses, complicationsmodule orthostatic hypotension, and

cardiac risk factors Determine frequency of follow-up—onthe basis of presence or absence of

Electrocardiography and rhythm complications and cardiac risk factorsstrip (R-R variation)—on thebasis of age and symptoms Consider more intensive cardiac

testing (such as stress test) or referralLipid profile (cholesterol, to cardiologist—on the basis of

triglycerides, high-density and findings on current examinationlow-density lipoproteins)

Renal module Module-specific follow-up Educate patient about renalassessment complications

Laboratory tests Determine frequency of follow-up—on•24-hour microalbuminuria the basis of presence or absence of•Creatinine clearance complications•Serum chemistry analysis

Refer to dietitian for instructions onmodifications of protein intake, ifneeded

Neuropathy module Module-specific follow-up Educate patient about neuropathologicassessment, including thorough complicationsfoot examination

Determine frequency of follow-up—onReview of symptoms relevant to the basis of presence or absence of

peripheral nerve and autonomic complicationsdysfunction

Refer to neurologist, if neededModule-specific testing•Vibratory sensation•Soft-touch•Pinprick