he primary efect attributed to gestational diabetes is exces sive fetal size or macrosomia that is variably defined and dis cussed further in Chapter 44 (p. 857). The perinatal goal is birth trauma associated with shoulder dystocia. In a retrospec tive analysis of more than 80,000 vaginal deliveries in Chinese women, Cheng and associates (2013) calculated a 76-fold greater risk for shoulder dystocia in newborns weighing :4200 g compared with the risk in those weighing <3500 g. Impor tantly, however, the odds ratio for shoulder dystocia in women with diabetes was <2. Although gestational diabetes is certainly a risk factor, it accounts for onl) a small number of pregnancies complicated by shoulder dystocia.
he excessive shoulder and trunk fat that commonly characterizes the macrosomic newborn of a diabetic mother theoretically predisposes such neonates to shoulder dystocia or cesarean delivery (Durnwald, 2004; McFarland, 2000). Landon and associates (2011) identified shoulder dystocia in approximately 4 percent of women with mild gestational diabetes compared with < 1 percent of women with a 50-g glucose screen result < 120 mg/dL. In a ptospective study of fetal adipose measurements, however, Buhling and coworkers (2012) demonstrated no diferences between measurements in 630 ofspring of women with gestational diabetes and 142 without diabetes. he authors attributed this negative inding to successful treatment of gestational diabetes.
Extensive evidence supports that insulin-like growth factors also playra role in fetal-growth regulation (Chap. 44, p. 845). hese proinsulin-like polypeptides are produced by virtually all fetal organs and are potent stimulators of cell diferentiation and division. Luo and coworkers (2012) reported that insulinlike growth factor-1 strongly correlated with birthweight. he HAPO study investigators also reported dramatic increases in cord-serum C-peptide levels with rising maternal glucose levels following a 75-g OGTT. C-peptide levels above the 90th percentile were found in almost a third of newborns in the highest glucose categories. Other factors implicated in macrosomia include epidermal growth factor, ibroblast growth factor, platelet-derived growth factor, leptin, and adiponectin (Grissa, 2010; Loukovaara, 2004; Mazaki-Tovi, 2005).
Hyperinsulinemia may provoke severe hypoglycemia within minutes of birth, but only three fourths of these episodes occur in the irst 6 hours (Harris, 2012). he deinition of neonatal hypoglycemia is controversial, with recommended clinical thresholds ranging from 35 to 45 mg/dL. An NIH workshop conference on neonatal hypoglycemia supported using a threshold of 35 mg/dL in term newborns but cautioned that this practice is not strictly evidence based (Hay, 2009). Newborns described by the HAPO study (2008) had an incidence of clinical neonatal hypoglycemia that rose with increasing maternal OGTT result values deined in Figure 57-6. The frequency varied from 1 to 2 percent, but it was as high as 4.6 percent in women with fasting glucose levels : 100 mg/ dL. Similarly,