Fetal Distress
Brenda A. Bucklin
Case Synopsis
An 18-year-old, 150-kg primigravida presents at 27 weeks’ gestation with severe
preeclampsia. Her worsening condition necessitates induction of labor. During uterine
contractions, the electronic fetal heart rate monitor demonstrates ominous changes
(Fig. 192-1).
PROBLEM ANALYSIS
Definition
Fetal distress is a widely used clinical term that is imprecise
and nonspecific. In 1998 the American College of
Obstetricians and Gynecologists (ACOG) published a com-
mittee opinion that suggested replacing the term fetal distress
with nonreassuring fetal heart rate tracing because the former
term has a low predictive value and is frequently associated
with the delivery of infants who turn out to be in good con-
dition. The ACOG went on to recommend that a nonreas-
suring fetal heart rate tracing be accompanied by a further
description of the findings (e.g., fetal bradycardia, repetitive
variable decelerations). Still, obstetricians continue to use
the term fetal distress to describe a wide range of fetal heart
rate abnormalities that, if not corrected or circumvented,
will result in decompensation of physiologic responses and
cause permanent central nervous system or other damage or
death. Anesthesiologists must consider the severity of the
fetal heart rate abnormality when determining the urgency
of delivery and the type of anesthesia to be administered.
Recognition
Consistent, accurate diagnosis of true fetal distress (i.e.,
intrauterine hypoxia or asphyxia) is a clinical challenge
because of the questionable reliability of electronic fetal
heart rate monitoring for predicting adverse neonatal out-
comes. Still, electronic fetal heart rate monitoring is the pri-
mary screening tool. Additional support for the diagnosis
may be obtained from the presence of meconium in the
amniotic fluid, deteriorating fetal acid-base status, lack of a
fetal heart rate response to acoustic or scalp stimulation, and
umbilical artery Doppler velocimetry. The most sensitive
indicators of fetal cerebral oxygenation are heart rate
variability or accelerations.
Gradual decreases in fetal oxygenation produce a variety
of fetal heart rate patterns (Fig. 192-2). Early signs of transient
hypoxemia in a neurologically intact fetus may include tachy-
cardia, persistent sinusoidal fetal heart rate pattern, and peri-
odic changes consisting of late and variable decelerations.
Although these changes alone do not preclude the delivery of
a healthy neonate, they should alert the clinician that the fetus
is at risk. In extreme cases, the fetus will lose all central influ-
ence over its heart rate and develop a straight-line tracing
770
192
devoid of accelerations, variability, and even deceleration
Abrupt and profound decreases in fetal oxygenation ofte
result in severe fetal bradycardia, usually less than 90 beats pe
minute. Ominous signs suggesting that both fetal acidosis an
hypoxia are present include the following:
● Loss of fetal heart rate accelerations
● Increase in baseline fetal heart rate
● Persistent absent variability, unresponsive to stimuli
● Absent variability with late or variable decelerations
The challenge for obstetricians is to judiciously conside
the electronic information within the clinical context t
ensure the best possible neonatal outcome. Emergenc
cesarean delivery is indicated when the condition is lif
threatening to the mother or fetus. In these situations, com
munication between obstetric and anesthesia care provider
is essential for maternal and fetal well-being.
Risk Assessment
The true incidence of fetal distress is difficult to quantif
largely because of the lack of clearly defined diagnostic cr
teria. However, it is a diagnosis that is likely overused b
physicians. In 1991 U.S. birth certificate statistics reveale
that fetal distress was a confounding factor in 4.3% of liv
births. More recently, rates of cesarean delivery for fetal dis
tress ranged from 2% to 8.7%.
Fetal distress may result from interference of oxyge
transport at the level of the mother, the placenta, the umbi
ical cord, or the fetus itself (Table 192-1). Sometimes th
cause is multifactorial, but more often a primary cause
identifiable. Common high-risk obstetric conditions tha
increase the risk of fetal distress include the following:
● Preeclampsia or eclampsia and chronic hypertension
● Diabetes mellitus
● Intrauterine growth retardation
● Oligohydramnios
● Fetal prematurity or postmaturity
● Chorioamnionitis
Implications
Severe and sustained hypoxia in the fetus will eventually lea
to profound acidosis, neurologic sequelae (e.g., seizure
coma, hypotonia), and ultimately, death.