Introduction and Overview of Perinatal Outcome

Introduction and Overview of Perinatal Outcome

Pregnancy produces major changes in metabolic fuels and hormones and in this way affects the management of diabetes. Basal hepatic glucose production

increases significantly with advancing gestation in lean or obese controls, but increased basal insulin secretion and fetal-placental utilization of glucose result in slightly lower fasting blood glucose levels. Fat deposition is accentuated in early pregnancy, but lipolysis is enhanced later in gestation, and more glycerol and free fatty acids (FFA) are released in the postabsorptive state (distant from meals). The increased FFA may contribute to the insulin resistance on glucose utilization by skeletal muscle during pregnancy. Ketogenesis is also accentuated in the postabsorptive state during pregnancy, probably due to increased provision of substrate FFA and hormonal effects on the maternal liver cells.

Despite increased first- and second-phase insulin release after a carbohy- drate load in normal pregnancy, in the fed state there is a significant reduction in net insulin-mediated glucose disposal by the third trimester. The result is somewhat higher maternal blood glucose levels in nondiabetic subjects, and marked hyperglycemia in inadequately treated pregnant diabetic women. The contra-insulin effects of gestation are related to hPL, progesterone, cortisol, and prolactin, with the defects at the postreceptor level of muscle and hepatic cells. Due to the insulin resistance and enhanced ketogenesis of pregnancy, ketoacidosis is a great danger during gestation. Markedly increased doses of insulin are usually required to control hyperglycemia after the first trimester. Glucagon is well suppressed by glucose during pregnancy, and secretory re- sponses of glucagon to amino acids are not increased above nonpregnant levels.

Fig. 1. Model of maternal gestational diabetes, fetal hyperinsulinemia, and infant out- come.

If diabetes is poorly controlled in the first weeks of pregnancy, the risks of spontaneous abortion and congenital malformation of the infant are increased considerably. Later in pregnancy, polyhydramnios is also common in women with poorly controlled diabetes and may lead to preterm delivery. Fetal hypoxia may develop in the third trimester if diabetic control has been inadequate. In such cases careful fetal monitoring must be used to prevent stillbirth. Maternal hyperglycemia and fetal hyperinsulinemia are associated with fetal macrosomia and delayed fetal lung maturation and inadequate production of surfactant apoprotein (fig. 1). Fetal macrosomia or large-for-dates (birth weight ?90th percentile for gestational age) increases the potential for traumatic vaginal If diabetes is poorly controlled in the first weeks of pregnancy, the risks of spontaneous abortion and congenital malformation of the infant are increased considerably. Later in pregnancy, polyhydramnios is also common in women with poorly controlled diabetes and may lead to preterm delivery. Fetal hypoxia may develop in the third trimester if diabetic control has been inadequate. In such cases careful fetal monitoring must be used to prevent stillbirth. Maternal hyperglycemia and fetal hyperinsulinemia are associated with fetal macrosomia and delayed fetal lung maturation and inadequate production of surfactant apoprotein (fig. 1). Fetal macrosomia or large-for-dates (birth weight ?90th percentile for gestational age) increases the potential for traumatic vaginal

Neonatal risks linked to poor maternal glycemic control include respira- tory distress syndrome, hypoglycemia, hyperbilirubinemia, hypocalcemia, and poor feeding. Although these problems are usually limited to the first days of life, excess glucose and b-hydroxybutyrate levels in utero have been related to diminished performance on psychomotor testing during childhood develop- ment. However, diabetic women have a ?90% chance of delivering a healthy child if they adhere to a program of careful dietary and glucose management.