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Chapter 21
Doppler Sonography in Pregnancies Complicated
with Pregestational Diabetes Mellitus
Dev Maulik, Genevieve Sicuranza, Andrzej Lysikiewicz, Reinaldo Figueroa
Introduction
During the past few decades, tremendous advances
have been made in the medical and obstetrical management
of pregnancies complicated with pregestational
diabetes resulting in considerable improvements
in maternal and perinatal outcomes [1]. Stringent
periconceptional glycemic control and advances
in fetal surveillance have significantly contributed to
this improvement. The successful management of a
pregestational diabetic mother requires timely and
appropriate antepartum fetal surveillance which permits
the pregnancy to progress while identifying the
fetus who may be compromised and may benefit
from delivery. Doppler velocimetry enables the investigation
of fetal circulatory decompensation, and thus
provides a noninvasive monitoring tool for assessing
fetal well-being. There is considerable evidence affirming
the efficacy of umbilical arterial Doppler sonography
in predicting and improving adverse perinatal
outcome in pregnancies with fetal growth restriction
(FGR) and preeclampsia; however, the utility
of Doppler fetal surveillance in managing uncomplicated
pregnancies with pregestational diabetes remains
controversial.
This chapter presents a review of the role of Doppler
sonography in assessing the fetus of a pregestational
diabetic mother and recommends a management
plan based on the current evidence.
Maternal Glycemic State
and Fetal Hemodynamics
Fetal circulatory response to altered maternal glycemic
state appears to be complex. This section briefly
addresses this issue pertaining to both hyper- and hypoglycemia.
In an experimental model involving late gestation
ewes, induction of acute maternal hyperglycemia produced
a 27%±29% reduction in the placental share of
the cardiac output which was redistributed to fetal
carcass, heart, renal, adrenal, and splanchnic circulations
[2]. Concordant with the changes in perfusion,
the fetuses also developed systemic hypoxemia and
mixed acidemia during induced maternal hyperglycemia
without any alterations in fetal cardiac, brain,
and renal oxygenation. The response to hyperglycemic
challenge, however, was different in the fetuses of
ewes rendered diabetic by streptozocin administration
[3]. The umbilical±placental blood flow did not
change significantly in these fetuses but significantly
declined in the controls, whereas fetal brain and renal
perfusion was significantly higher in the former at all
times than in the controls. The fetuses of the diabetic
mothers were also more hypoxemic than the controls.
Fetal hypoxemia induced by maternal hyperglycemia
could be explained by the earlier observation that
chronic fetal hyperglycemia is associated with accelerated
fetal oxidative metabolism. In the latter study,
chronic fetal hyperglycemia produced by fetal glucose
infusion via chronic in utero catheterization led to an
increase in calculated fetal O 2 consumption by approximately
30% (p