Professional Documents
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457
Review article
J. Perinat. Med.
29 (2001) 457464
1 Introduction
During delivery, it is not unusual for women to
have little or no nutrient intake in spite of the fact
that the demand for energy increases for skeletal
and smooth muscle contractions. The question remains as to what the optimal policy in nutritional
intake during labor should be. The major reason
for restricting oral intake is the possible risk or
aspiration of gastric contents leading to the Mendelson syndrome. In many countries, a totally restrictive policy is adhered to [14, 31] although in
recent years, there is a tendency towards a more
liberal policy. The American Society of Anesthesiologists, stated in 1999 that, during normal labor, parturients should be allowed to drink clear
liquids and in Great Britain an increasing number
of institutes allow eating or drinking during labor
[5, 50].
Mortality figures due to the Mendelson syndrome
in The Netherlands, where oral intake is left to
the decision of laboring women are, comparable
to that of countries where a restrictive policy is
adhered to [47, 50]. Although many authors of
review articles conclude that the restriction of
eating and drinking during labor should be reconsidered [5, 29, 33, 52, 55], little evidence is recorded on the actual effects of eating and drinking on the course of labor [22].
Maternal and fetal metabolism during labor has
been studied, but studies on the relationship to the
availability of energetic substrate and metabolic
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Conclusion: In most deliveries maternal blood glucose increases. A decline in maternal blood glucose can occur in long lasting deliveries without
adequate glucose supply, but this does not result in
severe hypoglycemia. Furthermore, due to the capacity of the placenta to regulate fetal glucose supply and fetal glucose sensitivity, it is unlikely that
fetal glucose supply will be jeopardized.
Fetal lactate is mostly of fetal origin, suggesting
fetal non-oxidative metabolism (a lack of oxygen). Hyperglycemia, however, may lead to an
increased production of lactate either in the maternal circulation and/or in the fetus/placenta. A
high maternal lactate furthermore diminishes the
ability of the fetus to transfer lactate to the maternal circulation. Combined with the increase in fetal oxygen consumption this may lead to a higher
risk of fetal acidemia.
4 Effects of fasting during labor and the
parallel to exercise
Deprivation of fluid and food during labor, theoretically, may have a negative impact on the progress
and outcome of labor. In animals, maternal and fetal blood glucose levels decline in fasting [54]. The
fetus is dependent upon glucose as its major energy
source and fetal activity has been shown to be
greater in higher maternal blood glucose levels
[32]. A lack of glucose, results in a higher mobilization of free fatty acids resulting in ketosis.
In pregnancy, the carbohydrate metabolism is altered [21]. There is a higher resistance to insulin
due to the effects of human placental lactogen,
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5 Glucose administration
To our knowledge, the only randomized controlled study on oral intake and maternal metabolic parameters has been published by Scrutton
et al [51]. They did not find a rise in maternal
lactate, nor maternal hyperglycemia, in women
who ate versus those who were starved. The formation of ketones was prevented by eating. Due
to the physiologic increase in the insulin concentration, it seems unlikely that oral intake can lead
to hyperglycemia in non-diabetic pregnant
women. Given the fact that most women in labor
do not eat or drink large amounts, oral caloric
intake is likely to be safe with regard to possible
effects on the fetal acid-base balance.
Conclusion: the infusion of hyperglycemic solutions may cause fetal acidemia. Using 510 %
glucose solutions would appear to be safe. Oral
supplementation of carbohydrates may be considered. It is unlikely that oral intake would cause
hyperglycemia, but relevant data is scarce.
Abstract
Aim: To discuss maternal and fetal metabolic events
during labor and the possible role of glucose administration.
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