Diabetes management for the primary care physician
Diabetes management for the primary care physician
By Indu Rao, MD
Stephen McDonald, MD
Until 1995, the only available oral agents in the United States were the sulfonylureas, limiting medical therapy for Type II diabetes to sulfonylureas and insulin. Over the last two years, several new medications with differing mechanisms of action have acquired approval by the U.S. Food and Drug Administration, allowing less frequent use of insulin.
Oral antidiabetic agents now target the pathophysiologic mechanisms of hyperglycemia, allowing a more rational management of Type II diabetes.1,2 (See Table 1, below.)
The two basic goals in the management of diabetes are control of hyperglycemia and screening and prevention of complications. Persistent hyperglycemia is the hallmark of diabetes and is responsible for the debilitating complications. Normalization or near-normalization of fasting and post-prandial glucose levels is the most important goal in the management of diabetes mellitus because it prevents acute and long-term complications.
The Diabetes Control and Complications Trial (DCCT) showed that intensive treatment to lower blood glucose delayed the onset and progression of microvascular complications in Type I diabetes.3 There is now growing evidence to show that this holds true for Type II diabetes as well.4-7
· Patient-centered care involves teamwork and training.
People with diabetes should receive their treatment and care from a physician-coordinated team. This includes physicians (primary care practitioners and sub-specialists), diabetic educators, nurses, dietitians, mental health professionals, and other resources as necessary. Patient education is of utmost importance, placing a major responsibility of care on the patient, and the value of continuing education by means of refresher courses should be encouraged.
· Meal-planning and exercise are cornerstones in diabetic management.
A standardized ADA diet is no longer recommended. Diabetics should be taught meal planning, and this should be tailored to fit as closely as possible to the patient's tastes, cultural preferences, convenience, and financial capabilities. A diabetic nutrition specialist may be consulted to aid with this aspect of treatment. The goal should be improved glucose, lipid, and blood pressure control. Even mild to moderate weight loss (5 to 10 kg) results in improved diabetic control.8
· Use these general guidelines to achieve nutritional goals in Type II diabetes:
- Space meals by spreading nutrient intake throughout the day.
- Use moderate caloric restriction of 250 to 500 calories less than average intake.
- Reduce total fat intake, especially saturated fats.
- Decrease cholesterol intake to less than 300 mg/d; if elevated LDL is present, decrease to 200 mg/d.
- Include 20 to 35 g of dietary fiber from a wide variety of food sources.
About 10% to 20% of the daily caloric intake should be derived from protein and the rest from fat and carbohydrates. The percentage of fat is dependent upon the lipid profile. With a normal lipid profile, total fat should supply less than 30% of calories, with less than 10% from saturated fat. The percentage from saturated fat should be further decreased to 7%, if elevated LDL is present. In the presence of elevated triglycerides, calories from total fat should be less than 20%, with less than 10% from saturated fat. More than 20% of calories should come from monosaturated fats.
· Follow these exercise recommendations:9
- Obtain an exercise stress electrocardiogram in patients over 35 before embarking on an exercise program.
- Start with mild exercises, such as walking or riding a stationary bike, and gradually increase exercise sessions.
- Include aerobic exercise at 50% to 70% of individual's maximum oxygen uptake lasting 20 to 45 minutes, three to four days per week.
- Encourage low intensity warm-up and cool-down exercises to improve flexibility and prevent injuries.
- Do not exercise when short of breath. Perceived exertion may be a better indicator of exercise intensity than the pulse rate.
Lifestyle modifications are essential
Although lifestyle modifications are a frustrating aspect of diabetic management, they are an essential part of glycemic control and improve blood glucose by decreasing insulin resistance and improving peripheral glucose use. Reinforce the value of meal planning and exercise at every visit.
· Failure of nonpharmacological therapy is an indication to start oral hypoglycemic medications.
In about two-thirds of Type II diabetics, blood glucose control will be achieved with diet and exercise.7 In the remaining one-third of patients, oral hypoglycemic agents will be necessary. If after three to six months of nonpharmacological therapy, the HbA1C remains above 7%, add an oral antidiabetic agent. When the FPG is above 200 mg/dL, an oral hypoglycemic agent may be started at the outset, in conjunction with lifestyle modifications.
With the array of medications now available, choice of initial therapy can be geared to suit the patient's profile.9,2 (See Table 2, below.) Oral hypoglycemic agents are used in conjunction with lifestyle modifications.
Initial monotherapy with sulfonylureas and metformin will undergo secondary failure at a rate of 5% to 10% per year.9 This will manifest as poor blood glucose control after three-to-five years of initially adequate control. When secondary failure occurs, combination therapy will be required. Principles guiding combination therapy:
- Do not substitute one drug for another but add a drug with a different mechanism of action.
- Add metformin or troglitazone, if fasting hyperglycemia is the main problem.
- Use acarbose or sufonylurea for post-prandial hyperglycemia.
Up to three oral medications with different mechanisms of action may be tried before instituting insulin therapy.1
· As beta-cell failure occurs, insulin will be required for effective blood glucose control.
Initially, the addition of a single injection of bedtime intermediate acting insulin or dinnertime combination insulin will control hyperglycemia.
The body mass index (BMI) may be used to choose the type of insulin therapy.10 In non-obese subjects (BMI is less than 30), use bedtime intermediate insulin (NPH/lente) along with daytime oral hypoglycemic agent.2,5 When the BMI is greater than 30, dinnertime 70/30 or other intermediate/regular combination insulin may control hyperglycemia.
Start with 10 to 15 units of intermediate-acting insulin insulin and increase by five units weekly until target glycemia achieved. If more than 35 units of insulin are required, troglitazone may be added to decrease insulin requirements. Metformin and acarbose may also be used in conjunction with insulin therapy.
In time, failure of single injection insulin will occur, and this is heralded by pre-dinner glucose values of more than 170 mg/dL. Multiple insulin injections will become necessary. At this point, individualized insulin regimens will need to be worked out, preferably in conjunction with an endocrinologist.
· Daily measurement of blood glucose by the patient, coupled with periodic HbA1C assessment is necessary to monitor the adequacy of glycemic control.
Self blood glucose monitoring (SMBG) at least two-to-three times per day provides the patient useful feedback regarding the success or failure of blood sugar control. Confirm the accuracy of patient results with simultaneous laboratory testing.
Hemoglobin A1C reflects glycemic control over a period of two-to-three months. It should be performed routinely in all diabetics. Obtain the first HbA1C level at the initial assessment. Then check the level every three months until the target level of 7% is achieved. Thereafter, it may be done semi-annually to ensure ongoing control of hyperglycemia.6
· Macrovascular complications.
Patients with Type II diabetes have had insulin resistance and impaired fasting glucose for many years prior to their diagnosis of diabetes. The insulin resistance syndrome (metabolic syndrome or syndrome X) includes hypertension, hypertrigly-ceridemia, low HDL levels, and abnormal fibrinolytic system, thus conferring enhanced atherogenecity.2,6
A two- to five-fold increase in the prevalence of cardiovascular, cerebrovascular, and peripheral vascular disease is seen in diabetics as compared to nondiabetics.
Diabetes is an independent major risk factor for atherosclerotic coronary artery disease.9 Other cardiovascular risk factors include hypertension, hyperlipidemia, smoking, and obesity through insulin resistance.
Ischemic heart disease occurs at a younger age in diabetics, affecting males and females alike. The atypical clinical manifestations of coronary artery disease in diabetics delay diagnostic and potentially lifesaving interventions. Myocardial infarction portends a poorer prognosis, and angioplasty results are less successful in diabetics. Aggressive cardiovascular risk factor reduction in diabetics is a must.
Recommendations for risk factor modification are as follows:6
·Check the blood pressure at every visit. Hypertension is present in one-third of patients at the time of diagnosis of Type II diabetes. The goal of therapy is to maintain blood pressure below 130/85 mmHg. This is achieved by weight loss, low sodium intake (less than 2 g/d), exercise, and decreased alcohol intake.
Antihypertensive medications of choice are angiotensin converting enzyme inhibitors (ACEI), calcium channel blockers, and alpha-1 blockers, as these medications do not have adverse effects on hyperglycemia or lipid profile. Use diuretics and beta-blockers with caution, as both worsen insulin resistance and the lipid profile. Beta-blockers confer a protective effect in patients who have had a myocardial infarction and therefore should not be withheld in this population.
· Obtain a fasting lipid profile annually.
Diabetes has an adverse effect on the lipid profile. The common abnormal lipid pattern in diabetics is elevated very low density lipoprotein (VLDL), a reduction in HDL, and an LDL portion that contains a greater proportion of small, dense, atherogenic LDL particles. Follow the NCEP (National Cholesterol Education Program Adult Treatment Panel II report) guidelines for treatment of dyslipidemia. This is based on the number of cardiovascular risk factors present and presence of coronary artery disease.11
· Microvascular complications.
- Diabetic retinopathy. Up to 21% of patients with Type II diabetes have retinopathy at the time of diagnosis. Five percent to 10% of Type II diabetics will become blind.9 The reasons for vision loss in patients with diabetic retinopathy include macular edema, retinal detachment, and vitreous hemorrhage.
Two other complications of diabetes, cataracts and glaucoma, can lead to visual loss. Patients with vision-threatening retinopathy may not have symptoms. Annual evaluation by means of dilated funduscopic examination is a valuable strategy because patients with asymptomatic macular edema and proliferative retinopathy can be identified.6 Timely intervention with laser photocoagulation in these patients can prevent visual loss.12
- Diabetic nephropathy. Twenty percent to 30% of Type II diabetics develop nephropathy, and one-fifth of these patients progress to end-stage renal disease. Evidence of diabetic nephropathy first presents as microalbuminuria. At this stage, dipstick urinalysis examination will be negative for protein.
For the detection of microalbuminuria, the spot collection method is easily performed in the office setting, although many physicians prefer to use a 24-hour collection of urine. As urinary albumin excretion rates increase, overt nephropathy develops.
Then the glomerular filtration rate falls, and patients eventually develop end-stage renal failure, requiring dialysis. Albuminuria is also a marker of greatly increased cardiovascular morbidity and mortality, and so aggressive intervention to reduce cardiovascular risk factors is indicated.
Annual screening for microalbuminuria is recommended. Interventions at the stage of microalbuminuria effectively delay the progression to overt nephropathy and renal failure.6 These include:
1. strict glycemic control;
2. control of hypertension;
3. use of ACEI;
4. restriction of protein intake to 0.8 g/kg/d with the onset of overt nephropathy;
5. referral to nephrologist when GFR is less than 70 mL/min or serum creatinine is greater than 2 mg /dL.
· Diabetic foot care.
Unperceived, excessive, and repetitive pressure on plantar bony surfaces due to the presence of sensory neuropathy predisposes to neuropathic foot ulcers and joint destruction (Charcot's joint).
A history of previous ulcers or infections further increases the risk of ulcer development and progression to lower extremity amputation. Once amputation of one limb has occurred, the prognosis for the contralateral limb is poor. Appropriate screening and intervention can prevent diabetic foot ulcers.6,13
A simple method to test the presence of sensory neuropathy is the use of a 10 g nylon monofilament. This is pressed against the skin to the point of buckling. Patients who cannot feel the monofilament are at risk for ulceration and require special care that entails education in lifelong foot care, therapeutic footwear, and periodic callus and nail care.13 Annual screening using the sensory monofilament for loss of protective sensation is recommended.
Summary
Diabetes is a common, chronic disease that is serious, treatable, and undertreated. Primary care providers treat the large majority (less than 90%) of Type II diabetics. With the new diagnostic criteria, an effort should be made to identify all diabetics who would benefit from early treatment to prevent debilitating complications.
Understanding the pathophysiology provides a rational basis for the efficient control of blood sugar using the various oral hypoglycemics that are currently available. (See Figure 1 for an algorithm of diabetes in perspective, below.)
Tight control of blood glucose is paramount. Early detection of complications should prompt interventions that prevent their progression to blindness, renal failure, or amputations. Cardiac disease is the major cause of death in Type II diabetes; aggressive cardiovascular risk factor modification is mandatory. Finally a team-oriented approach to management is beneficial, and the most critical member of the team is the patient.
· Indu Rao, MD, is the Clara Wifenbach Fellow in Women's Health at the Kettering Medical Center, Dayton, OH.
· Stephen D. McDonald, MD, is an endocrinologist and program director of the Internal Medicine Residency at the Kettering Medical Center, Wright State University, Dayton, OH.
References
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2. Bressler R, Johnson DG. Pharmacological regulation of blood glucose levels in NIDDM. Arch Intern Med 1997; 157:836-848.
3. The Diabetes Control and Complications Trial Research Group. The effect of intensive treatment of diabetes on the development and progression of long-term complications in IDDM. N Engl J Med 1993; 329:977-986.
4. Ohkubo Y, et al. Intensive insulin therapy prevents the progression of diabetic macrovascular complications in Japanese patients with NIDDM: A randomized prospective 6-year study. Diabetes Res Clin Pract 1995; 28:103-117.
5. Henry RR, Genurth S. Forum One: Current recommendations about intensification of metabolic control in NIDDM. Ann Intern Med 1996; 124:175-177.
6. American Diabetes Association. Standards of medical care for patients mellitus. Diabetes Care 1997; 20(Suppl):S5-S70.
7. Pollet RJ, El-Kebbi I. The applicability and implications of the DCCT to NIDDM. Diabetes Rev 1994; 2:413-427.
8. Maggio CA, Pi-Sunyer FX. The prevention and treatment of obesity: Application to Type II diabetes. Diabetes Care 1997; 20:1,774-1,860.
9. Harris M, Couric C, Reiber G, et al (eds). Diabetes in America. 2nd ed. Washington DC: U.S. Government Printing Office; 1995 (NIH publication No. 95-1468).
10. Riddle, MC, Hart J, Bingham P, et al. Combined therapy for obese Type II diabetes: Suppertime mixed insulin with daytime sulfonylurea. Am J Med Sci 1992; 303:151-156.
11. Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults, NCEP II. JAMA 1993; 269:3,015-3,023.
12. Clark CM, Lee DA. Prevention and treatment of the complications of diabetes mellitus. N Engl J Med 1995; 332:1,210-1,216.
13. Caputo GG, et al. Assessment of foot disease in patients with diabetes. N Engl J Med 1994; 331:854-860.
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