Infants of diabetic mothers. Fetal and neonatal pathophysiology.

Abstract

Most of the clinical problems experienced by the IDM in the immediate neonatal period are manifestations of abnormal fetal developmental physiology that occur in response to an increased flux of glucose from mother to fetus. The principal fetal responses are hyperglycemia, hyperinsulinemia, increased metabolic rate, and hypoxemia. Those fetal responses very likely lead to a redistribution of cardiac output, increased release of norepinephrine, and blunted release of glucagon. More fat is stored in adipocytes; more glycogen is stored in the liver; the heart may develop asymmetric septal hypertrophy; and lung metabolism is altered to delay the appearance of mature surfactant. At birth, the macrosomic IDM develops hypoglycemia that has a multifactorial basis (hyperinsulinemia, hypoglucagonemia, and probably diminished gluconeogenic and cortisol production rates). The IDM may experience respiratory symptoms from one of three causes: IRDS, persistent pulmonary hypertension, or congestive heart failure. Hyperbilirubinemia may occur because of increased rate of hemolysis; hypocalcemia and hypomagnesemia are likely within the first 3 days in association with a sluggish PTH response; and abnormal levels of inhibitors of fibrinolysis and platelet prostaglandin E-like substances may stimulate abnormal thrombosis.