Overview of fetal assessment

Overview of fetal assessment

Authors
Caroline Signore, MD, MPH
Catherine Spong, MD
Section Editor
Susan M Ramin, MD
Deputy Editor
Vanessa A Barss, MD
Disclosures
All topics are updated as new evidence becomes available and our peer review process is
complete.
Literature review current through: Oct 2012. | This topic last updated: Nov 15, 2012.
INTRODUCTION The primary goal of antenatal testing is to identify fetuses at risk of
intrauterine neurologic injury or death so that these adverse outcomes can be prevented. Many
techniques for assessment of fetal well-being have been introduced into clinical practice,
beginning in the 1970s (table 1). Despite widespread use of these techniques, there is limited
evidence to guide their optimal use or to demonstrate their effectiveness at improving perinatal
outcomes.
This topic will provide an overview of fetal assessment. Detailed discussions of the various
techniques used and conditions where antenatal assessment is indicated are available separately.
(See individual topic reviews).
RATIONALE Fetal hypoxia and acidosis represent the final common pathway to fetal injury
and death in many high risk pregnancies [1]. The basis for antepartum testing is the premise that
the fetus whose oxygenation in utero is challenged will respond with a series of detectable
physiologic adaptive or decompensatory signs as hypoxemia or frank metabolic acidemia
develop (figure 1). For example:
Blood flow is directed to the brain, heart, and adrenals and away from the kidney. The
reduction in renal perfusion leads to decreased fetal urine production, which results in
decreased amniotic fluid volume.
Fetal movements decrease as the fetus attempts to conserve energy [2]. The loss of fetal
movement can be a sign of ongoing central nervous system hypoxia and injury.
A chemoreceptor response to hypoxemia leads to vagally-mediated reflex slowing of the
fetal heart rate (FHR), which may appear clinically as late decelerations associated with
uterine contractions.
A number of investigators have described sequences of measurable changes in fetal blood flow
and biophysical parameters that occur as placental insufficiency worsens and fetal hypoxemia
and acidemia develop [3,4]. Although the precise sequences of observed characteristics differ
slightly in these reports, a general pattern of fetal response to intrauterine challenge emerges:
loss of FHR reactivity (nonreactive nonstress test) and abnormal blood flow in the umbilical
artery (absent or reversed end-diastolic flow) are often the earliest signs of fetal compromise.
Sequential changes in other fetal vessels (middle cerebral artery, venous circulation) are
detectable next, followed by abnormalities in biophysical parameters such as fetal breathing
movements, fetal body movements, and fetal tone. However, not all fetuses who exhibit the full
range of these findings will exhibit significant metabolic acidosis at birth [5].
ANTENATAL TESTING METHODS
Fetal movement counting Fetal movements are usually first perceptible to the mother at 17 to
20 weeks (termed quickening) and become more prominent as gestation advances. When
correlated sonographically, about 50 percent of isolated limb movements are perceived by the
mother, whereas 80 percent of trunk and limb movements are perceived [6].
Fetal movement decreases in response to hypoxemia, making formalized maternal assessment of
fetal movements a potentially simple method of monitoring fetal oxygenation and well-being.
However, existing evidence does not support any specific fetal movement threshold or "alarm
limit" below which fetal risk is increased.
Results of trials of routine fetal movement assessment for reduction of stillbirth have been
mixed. In a randomized trial conducted in Denmark, fetal movement counting was associated
with a 73 percent reduction in avoidable stillbirths (RR 0.27, 95% CI 0.08-0.93) [7]. In contrast,
a subsequent large (N = 68,654) international trial found no significant difference in potentially
avoidable late fetal deaths between women who were instructed to count routinely and controls
[8]. A systematic review concluded that there was insufficient evidence to recommend routine
fetal movement counting to prevent stillbirth [9].
An approach to counseling women about monitoring fetal activity and evaluation of women with
decreased fetal activity can be found separately. (See "Evaluation of decreased fetal
movements".)
Contraction stress test The contraction stress test (CST) is based on the premise that uterine
contractions transiently restrict oxygen delivery to the fetus and that a hypoxic fetus will
demonstrate recurrent late decelerations (waveform 1 and table 1). (See "Antepartum fetal heart
rate assessment", section on 'Cardiovascular response to hypoxia'.)
The rate of antepartum stillbirth within one week of a negative CST (ie, the false negative rate) is
0.04 percent, thus providing reassurance of fetal well-being [10]. After a positive CST, however,
up to 30 percent of patients have been reported to tolerate labor without FHR changes
necessitating intervention [11].
Assessment of FHR reactivity can help differentiate false-positive from true-positive CSTs. In
one study, 50 percent of reactive positive CSTs were false positives, but 100 percent of non-
reactive positive CSTs were true positives, ie, intrapartum FHR was non-reassuring [12].
Overall, the high false positive rate, as well as the need to stimulate contractions and the fact that
inducing contractions is contraindicated in a number of conditions (eg, placenta previa), are
major drawbacks to use of the CST (table 1). (See "Antepartum fetal heart rate assessment",
section on 'Contraction stress test'.)