TABLE 57-4. Diagnosis of Overt Diabetes in Pregnancya
Measure of Glycemia Threshold
Fasting plasma glucose At least 7.0 mmollL (126 mg/dL) Hemoglobin Ale At least 6.5% Random plasma glucose At least 11.1 mmol/L (200 mg/dL) plus confirmation aApply to women without known diabetes antedating pregnancy. The decision to perform blood testing for evaluation of glycemia all pregnant women r only on women with characteristics indicating a high risk for diabetes is based on the background frequency of abnormal glucose metabolism in the population and on local circumstances.
Data from International Association of Diabetes and Pregnancy Study Groups Consensus
Panel, 201n0.
Preterm Delivery. Overt diabetes is an undisputed risk factor for preterm birth. Eidem and associates (2011) analyzed 1307 births in women with type 1 diabetes from the Norwegian NIedical Birth Registry. More than 26 percent were delivered preterm compared with 6.8 percent in the general obstetrical population. Moreover, almost 60 percent were indicated preterm births, that is, due to obstetrical or medical complications. In one review of more than 500,000 California births, 19 percent of women with pregestational diabetes had a preterm birth compared with 9 percent in controls (Yanit, 2012). In the Canadian study shown in Table 57-5, the incidence of preterm birth was 28 percent.
Malformations. he incidence of major malformations in women with type 1 diabetes is at least doubled and approximates 11 percent Qovanovic, 2015). These account for almost half of perinatal deaths in diabetic pregnancies. As shown in Table 57-6, cardiovascular malformations accounted for more than half of the anomalies. In a cohort study of more than 2 million births in Canada, the risk of an isolated cardiac defect was ivefold higher in women with type 1 diabetes (Uu, 2013). he caudal regression sequence, described in Chapter 10 (p. 196), is a rare malformation frequently associated with maternal diabetes (Garne, 2012).
Poorly controlled diabetes, both preconceptionally and early in pregnancy, is thought to underlie this elevated severemalformation risk. s shown in Figure 57-2, increased maternal HbA[c levels and major malformations clearly correlate. To explain this, at least three interrelated molecular chain reactions have been linked to maternal hyperglycemia (Reece, 2012). hese include alterations in cellular lipid metabolism, excess production of toxic superoxide radicals, and activation of programmed cell death. In their review of molecular mechanisms underlying diabetic embryopathy, Yang and colleagues (2015) suggest that these cellular responses to oxidative stress represent potential therapeutic targets to prevent diabetes-induced embryopathy.
Altered Fetal Growth. Diminished growth may result from congenitl malformations or from substrate deprivation due to advanced maternal vascular disease. That said, fetal overgrowth is more typical of pregestational diabetes. Maternal hyperglycemia prompts fetal hyperinsulinemia, and this in turn stimulates excessive somatic growth. Except for the brain, most fetal organs are afected by the macrosomia that characterizes the fetus of a diabetic woman. Newborns such as the one shown in Figure 57-3 are described as being anthropometrically diferent from other largefor-gestational age (LGA) neonates (Catalano, 2003; Durnwald, 2004). Speciically, those whose mothers are diabetic have excesyrsive fat deposition on the shoulders and trunk, which predisposes to shoulder dystocia or cesarean delivery.