In pregnancies complicated by diabetes mellitus, chronic maternal hyperglycemia exposes the fetus to elevated glucose levels that freely cross the placenta via facilitated diffusion (GLUT-1 transporters). Maternal insulin does not cross the placenta, so the fetal pancreatic beta cells undergo hyperplasia and hypertrophy, producing excessive insulin. Fetal hyperinsulinism acts as a growth factor, causing macrosomia, organomegaly (cardiomegaly, hepatomegaly), and increased adipose deposition. At birth, the maternal glucose supply is abruptly removed, but the neonatal pancreas continues to secrete supraphysiological insulin levels, causing rapid and potentially severe hypoglycemia within the first 1-4 hours of life. Additional metabolic complications include hypocalcemia (impaired parathyroid response), hypomagnesemia, polycythemia (erythropoietin response to chronic fetal hypoxia), hyperbilirubinemia (from polycythemia breakdown), and respiratory distress syndrome (insulin inhibits surfactant production). The nurse implements comprehensive metabolic monitoring, manages glucose stabilization, coordinates diagnostic workup, and provides family education.