Aim: To discuss maternal and fetal metabolic events during labor and the possible role of glucose administration.
Results: The oxidative pathway covers the largest part of the energy demand of labor, although in the second stage or, in polysystolic labor, the non-oxidative pathway becomes important as well. Glucose is the main maternal energy source, but the rise in ketobodies, even during normal labor, suggests a relative shortage. In the first stage of labor, a combination of a respiratory alkalosis, and to a lesser extent, a metabolic acidosis, result in a rise in the maternal pH. In the second stage of labor, the maternal pH decreases due to an increasing metabolic acidosis. Glucose is also the main fetal energetic fuel. In fetal hypoxia, lactate is produced, which in most cases is transferred to the maternal circulation. High maternal lactate concentrations, however, may interfere with this process. Furthermore, fetal hyperglycemia may lead to an increased fetal lactate production.
Conclusions: Maternal hyperglycemia, may lead to an increase in maternal and fetal lactate production resulting in metabolic acidosis. Unlike high dosage intravenous glucose administration, it is not likely that oral intake of carbohydrates leads to maternal and fetal hyperglycemia and subsequently to metabolic acidosis, but studies are rare.