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The prevalence of GDM is estimated to be about 2%. GDM is usually identified by prenatal screening of preg-nant patients. It may be suspected, however, in patients with known risk factors for GDM, which include age, ethnicity, past obstetric history (gestational diabetes in a previous pregnancy, a history of an infant weighing more than 4000 g at birth, repeated spontaneous abor-tions, or a history of unexplained stillbirth), a strong fam-ily history of diabetes, and obesity. However, 50% of patients identified as having gestational diabetes do not have such risk factors.
The most commonly used screening test for glucose intoler-ance during pregnancy is given at 24 to 28 weeks of gesta-tion and consists of a 50-g, 1-hour oral glucose challenge.
Patients whose glucose value exceeds 140 mg/dL (some use 130 or 135 mg/dL) require a standard 3-hour glucose tolerance test using 100 g of glucose. Two or more abnor-mal results of the 3-hour test establish the diagnosis of gestational diabetes.
In patients lacking any risk factors, the 1-hour glucose screening is usually performed between 24 and 28 weeks of gestation because glucose intolerance is generally evident by that time. Using this screening method, approximately 15% of patients have an abnormal screening test. Of those patients who then proceed to have the standard 3-hour oral glucose tolerance test, approximately 15% are diagnosed as having gestational diabetes. Although many practitio-ners choose to screen high-risk patients early in pregnancy, the benefit of early treatment of women with GDM iden-tified early in pregnancy has not been demonstrated, but, rather, has been accepted on a theoretical basis.
There is currently insufficient evidence to determine the optimal antepartum testing regimen for women with relatively normal glucose levels on diet therapy and no other risk factors. Despitethe lack of evidence, it is reasonable to conclude that women whose GDM is not well-controlled, who require insulin, or have other risk factors such as hypertension should receive the same antepartum testing regimen as women with pregestational diabetes. While ultrasonogra-phy can be used to assess congenital anomalies, the reliabil-ity of ultrasonography to estimate fetal weight and predict macrosomia prior to delivery has not been established.
Often overlooked or underemphasized in the overall manage-ment of a patient whose pregnancy is complicated by diabetes mellitus is the importance of patient education. The patientwith newly diagnosed diabetes should receive general dia-betic counseling, along with information about the unique features of the combination of diabetes and pregnancy. Home glucose monitoring is the norm, and instruction in technique should be provided.
The overall goal of managing GDM is to control glu-cose values within circumscribed limits: fasting glucose levels of less than 95 mg/dL or 1-hour postprandial levels of 130 to 140 mg/dL or 2-hour postprandial values less than 120 mg/dL. The mainstay of GDM management is diet. The recommended diet is about 30 Kcal/kg/day of ideal body weight, composed of approximately 45% complex carbohydrates, 35% fat, and 20% protein. With carefulattention to diet, many mothers with GDM do not require insulin. Current available evidence does not support arecommendation for or against moderate caloric restric-tion in obese women with GDM. However, if caloric re-striction is used, the diet should be restricted by no more than 33% of calories.
Patients are instructed to obtain a morning fasting glucose, along with pre- and postprandial glucose values throughout the day and evening. The precise goals for glucose control vary, but in general the fasting plasma glu-cose should be maintained in the 90 to 100 mg/100 mL range, and the postprandial values obtained throughout the day at <120 to 140 mg/100 mL. For those patients who are able to control their gestational diabetes with diet alone, the perinatal outcome is good. Pregnancy is allowed to continue to term, with delivery planned at that time.
For patients with GDM whose glucose levels cannot be con-trolled with diet, exogenous insulin is needed. Frequently, acombination of intermediate-acting NPH (neutral prot-amine Hagedorn) and fast-acting insulin (such as regular or lispro) is used together near breakfast and dinner in order to suppress gluconeogenesis in the liver as well as to counter the rises in glucose that occur with meals. This necessitates only twice-daily injections. However, some advocate split-ting the evening insulin dose, giving the short-acting in-sulin at dinner, and then NPH at bedtime, in order to decrease the risk of nocturnal hypoglycemia. Insulin does notcross the placenta and, therefore, does not directly affect the fetus. However, glucose does cross the placenta (by facilitated dif-fusion); the higher the maternal glucose level, the higher the fetal glucose level. In response, the fetus produces more insulin. This increased insulin production converts glucose to fat, resulting in the heavier infants (macrosomia) often noted in patients with diabetes. Following delivery, the high maternal glucose transfer ceases, but the continuing high fetal insulin concentration may lead to significant neonatal hypoglycemia temporarily.
Therapy with oral hypoglycemic agents is a newer aspect of diabetic therapy, and these agents are being used more commonly in pregnancy. Glyburide, which does not cross the placenta, has been shown to be comparable to insulin in both glucose control and adverse maternal and neonatal outcomes. Metformin has been used in many patients with polycystic ovary syndrome to achieve preg-nancy, but is not used regularly after the first trimester for glucose control. As with pregestational diabetes, the use of these agents should be carefully considered and individualized.
Patients with diabetes are monitored closely throughout pregnancy, usually at 1- to 2-week intervals. Insulin adjust-ments are made on the basis of the glucose logs main-tained by the patient. Also, as previously described, insulin requirements of a pregnant patient are expected to increase as pregnancy advances because of the rising production of hPL by the placenta, with its insulin-resistant effect.
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