Despite improved outcome as reflected in the dramatic decline in maternal and perinatal morbidity and mortality over the past few decades, controversy still exists regarding the care of pregnant women with gestational diabetes mellitus (GDM). Carbohydrate intolerance is the most common metabolic complication of pregnancy, with an incidence that varies from 1 to 5%. When not diagnosed, or when treated inappropriately, GDM is associated with an adverse maternal and fetal outcome, such as large-for-gestational age infant, macrosomia, cesarean section, stillbirth, and neonatal, childhood, and adult complications. An increasing body of evidence supports the hypothesis that certain developing tissues and organs in the fetus of the diabetic mother may receive an imprint of the abnormal gestational milieu, and this imprint can have permanent long-range implications for function after birth. The fetal tissues most likely to be affected are neural cells, adipocytes, muscle cells, and pancreatic β-cells. During the third trimester (when diabetes is usually diagnosed), the proliferation of fetal adipocytes, muscle cells, pancreatic β-cells, and neuroendocrine cells is the basis for the development later in life of obesity or non-insulin-dependent diabetes mellitus. Metabolic alterations during parturition are responsible for transient neonatal metabolic complications, such as hypoglycemia, hypocalcemia, and hypomagnesemia. Fetal hyperinsulinemia leads to a decreased level of arterial oxygen and an increase in plasma erythropoietin concentration. The chronic hypoxemic state in utero may explain some cases of intrauterine fetal death, as well as fetal polycythemia, hyperbilirubinemia, and renal vein thrombosis. These complications, together with the increased rate of labor complications (shoulder dystocia, birth trauma) and cesarean sections, contribute to the higher maternal morbidity and mortality among diabetic patients as well as a high risk of diabetes later in life.
|Number of pages||12|
|State||Published - 1995|