INTRODUCTION
Diabetes is a metabolic disease characterized by hyperglycemia resulting from defects in insulin secretion or insulin action or both.
About 3-10% of pregnant mothers are suffering from diabetes. Depending Recent studies suggest that the prevalence of diabetes among women of childbearing age is increasing in the world. This increase is believed to be attributable to
1. more sedentary lifestyles,
2. changes in diet,
3. the virtual epidemic of childhood and adolescent obesity
Although 80% or more of this glucose intolerance during pregnancy occurs in women with gestational diabetes mellitus (GDM), the associated fetal and newborn morbidity rates are disproportionate.
Infants of mothers with preexisting diabetes experience double the risk of serious injury at birth, triple the likelihood of cesarean delivery, and quadruple the incidence of newborn intensive care unit admission. Recent studies indicate that the risk of these morbidities in individual cases is proportional to the degree of maternal hyperglycemia. For this reason, the excessive fetal and neonatal morbidity attributable to diabetes in pregnancy should be considered preventable.
The prevalence of gestational diabetes is strongly related to the patient's race and culture.
• Typically, only 1.5-2% of white persons from the mid western United States develop GDM, while American Indians from the southwestern United States may have rates as high as 15%.
• In Hispanic, African American, and Asian populations, the rate is 5-8%.
PATHOPHYSIOLOGY (HOW DOES IT HAPPENS)
Normal metabolism during pregnancy
The goal of metabolism during pregnancy is to ensure that an ample, but not excessive, supply of glucose is available to the mother and fetus. To achieve this goal with each feeding, the pregnant woman undergoes a complex series of maternal hormonal actions:
1. a rise in blood glucose,and
2. the secondary secretion of pancreatic insulin, glucagon, somatomedins, and adrenal catecholamines.
The key features of this complex interaction include the following:
• A pregnant woman has a tendency to develop low sugar level (hypoglycemia) between meals and during sleep than that of nonpregnant woman because the fetus continues to draw glucose across the placenta from the maternal bloodstream, even during periods of fasting.
• The mean insulin level is 50% higher during last trimester than that of nonpregnant. This due to the high levels of placental steroid and peptide hormones (eg, estrogens, progesterone, chorionic somatomammotropin). These hormones increase the tissue resistance to insulin therefore insulin secretion is increased
• If insulin secretion is inadequate, both the mother and fetus develop high sugar levels (hyperglycemia). This can lead to accelerated fetal growth, which can bring many fetal and maternal complications
During a healthy pregnancy, mean fasting blood sugar levels decline progressively to a remarkably low value of 74 ± 2.7 (standard deviation) mg/dL. On the other hand, peak postprandial blood sugar values rarely exceed 120 mg/dL. Meticulous replication of the normal glycemic profile during pregnancy has been demonstrated to reduce the rate of macrosomia (large fetus). Specifically, when 2-hour postprandial glucose levels are maintained at less than 120 mg/dL, approximately 20% of fetuses demonstrate macrosomia. Conversely, if postprandial levels range up to 160 mg/dL, macrosomia rates rise to 35%.
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