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CHAPTER 2 Prenatal Environment: Effect on Neonatal Outcome
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29
MATERNAL NUTRITION,
MALNUTRITION, AND OBESITY
Maternal nutritional status and placental function during pregnancy can significantly influence the growth, development, and health of
the fetus and newborn. Nutritional problems that
interfere with fetal cell division (increases in cell
number) can have permanent consequences. If the
fetus is at a stage in which cells are only enlarging (increases in cell size), nutritional deficits may
be reversed if a healthy maternal dietary intake is
resumed soon enough in the pregnancy. All women
presenting for prenatal care should be questioned
about their usual dietary intake and should have
their weight and height assessed so that body mass
index (BMI) can be determined and appropriate
nutrition counseling initiated.
138
BMI can be calculated by dividing a woman’s prepregnancy weight
in kilograms by her height in meters squared; it is
the most frequently used single tool in determining obesity. If a woman’s prepregnancy weight is
unknown, the value obtained at the first prenatal
visit should be used. Although the BMI values for
classification vary, the Institute of Medicine (IOM)
employs the relative weight classification and prepregnancy BMI values as follows86:
• Underweight: less than 18.5
• Healthy weight: 18.5 to 24.9
• Overweight: 25 to 29.9
• Obese: greater than or equal to 30
Optimal ranges for weight gain in singleton
pregnancies are also based on the IOM recommendations. As a general rule, weight gain should be as
follows: underweight women should gain 28 to 40
lb; normal-weight women, 25 to 35 lb; overweight
women, 15 to 25 lb; obese women, 11 to 20 lb. The
optimal weight gain for women carrying twins is
35 to 45 lb.86 The IOM guidelines are continually
being evaluated, but at least one study confirms
that following these guidelines can improve pregnancy outcomes. However, fewer than one-half
of women gain the recommended weight during
pregnancy, with 43.3% of women gaining above the
IOM guidelines.
147
Excessive weight gain in obese
women is highly associated with an increased risk of
emergency cesarean delivery.96A recent study found
that the strongest predictor of pregnancy outcome
was the amount of gestational weight gain rather
than the presence of GDM.27 Excessive gestational
weight gain is an independent factor for fetal macrosomia and birth at less than 37 weeks.
Prenatal nutrition involves more than appropriate weight gain; a variety of healthy foods should
be consumed, providing essential nutrients.
169
The
dietary reference intakes increase for most nutrients during pregnancy. Protein, iron, vitamin A,
and iodine requirements nearly double, yet some
nutrient requirements do not change much.
157
Other maternal factors that should be considered
when counseling women on nutrition include age,
parity, preconceptual nutritional status, preexisting
medical conditions, current medical conditions
complicating the pregnancy, food likes and dislikes,
and cultural influences. Each woman’s counseling
should be individualized, and referral to a nutrition specialist and other medical specialists may be
indicated.
Malnourished and underweight mothers have
more perinatal losses and preterm births, and their
newborns have lower Apgar scores and more
frequently are of low birth weight (<2500 g).
This is especially true of significantly underweight women (low BMI) and women with
eating disorders, such as anorexia and bulimia,
who fail to gain adequate weight during preg-
119,166
nancy.
SGA newborns, defined as below the
10th percentile birth weight for gestational age, have
higher mortality rates in the perinatal period and
are at risk for later problems, such as insulin resistance and poor school performance.
166
However, it
may be difficult to draw direct correlations between
inadequate maternal diet and fetal growth unless
the nutritional disturbances are severe. Many fetuses
grow well despite suboptimal maternal nutrition, in
part because of the complexities of placental transport and the ability of the fetus to be preferentially
supplied with some nutrients.
Although reduced birth weight is associated with
inadequate carbohydrate, protein, and total caloric
intake, inappropriate amounts of other nutrients
may also affect the fetus. Vitamin and mineral
deficiencies have been linked to miscarriage and
stillbirth, congestive heart failure (thiamine), megaloblastic anemia (folic acid, vitamin B12), congenital
anomalies, including neural tube defects (folic acid,
zinc, copper), and skeletal abnormalities (vitamin D,
calcium).
49,65,158
Recently, a plethora of evidence has been published
about the impact of maternal vitamin D deficiency
and an association with poor pregnancy outcomes
such as preterm birth, preeclampsia, GDM, perinatal
depression, SGA infants, and asthma symptoms in
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offspring.
138
However, RCTs of vitamin D supplementation to improve perinatal outcomes has
resulted in conflicting evidence because of a lack of
consistency with dosing regimens and differing gestational ages when supplementation was initiated.
One important result of the multiple meta-analyses
that have been published about vitamin D supplementation in pregnancy is that there were no
incidences of vitamin D toxicity despite using doses
as high as 200,000 units intramuscular injection.
138
Women who become pregnant after surgery are
at increased risk for nutritional deficiencies and
require close monitoring.
97,149
The current guidelines from the American College of Obstetricians
and Gynecologists (ACOG),9 the American Society
of Metabolic and Bariatric Surgery, the Obesity
Society, and the American Association of Clinical
Endocrinology
110
recommend delaying pregnancy for at a minimum of 12 to 18 months after
bariatric surgery.97 Recent meta-analysis shows
a decreased risk of GDM, large-for-gestationalage (LGA) infants, gestational hypertension, all
hypertensive disorders, postpartum hemorrhage,
and cesarean delivery rates in pregnant women after
bariatric surgery.97 However, there is an increased
risk of SGA infants, IUGR, and preterm birth after
bariatric surgery.
Obesity is not only an epidemic in the United
States and other developed countries, but is a
major problem globally.
21,171
Public health officials
now cite obesity as the leading health problem
confronting women today. Obesity is a complex
problem resulting from a combination of genetic,
cultural, behavioral, socioeconomic, and environmental influences. Obesity affects all organ systems
and contributes to a multitude of physiologic
complications, such as cardiovascular disease, GDM,
infections, preeclampsia, and other adverse perinatal
outcomes.
116,171
Approximately 30% of pregnant women are
obese (BMI ≥30) and at risk for perinatal compli-
116
cations.
Overweight, obese, and morbidly obese
women (BMI >40) are at risk for chorioamnionitis,
preeclampsia, stillbirth, cesarean delivery, instrumental delivery, postpartum hemorrhage, perineal
lacerations, and prolonged hospital stay.
21,171
Their
offspring may suffer macrosomia, shoulder
dystocia, meconium aspiration, fetal distress,
preterm birth, early neonatal death, abnormal
labor, complications from cesarean birth, birth
defects, and higher risk of admission to the
116,171
NICU.
A 1% decrease in the number of obese
pregnant women in the United States would result
in 16,000 fewer cesarean births per year.
44
In addition, obese women may be struggling
with associated psychosocial problems, such as poor
self-esteem, guilt about weight, depression, and ridicule from family and others. Some may not seek
prenatal care until pregnancy is well into the second
or third trimester. Thus obese women should be
considered at high risk for childbearing complications, and these women and their fetus/newborn
should be monitored closely throughout gestation
and the perinatal period. Preconception or early
pregnancy dietary counseling, taking into account
the increased risk of GDM for women with obesity,
and promoting routine exercise and sleep hygiene
can improve maternal health and pregnancy outcomes. Women with obesity are less likely to stay
within the gestational weight gain recommendations, yet staying within weight gain guidelines
promotes normal birth weight (appropriate for
gestational age) and improves perinatal outcomes.
116
In conclusion, maternal health behavior, including smoking, problems with nutrition, and drug
use, before and during pregnancy is associated
with adverse outcomes for the newborn and also
long-term health risks of the newborn well into
adulthood. Supportive, informed prenatal care for
pregnant women at risk is essential to improved
newborn health.
Obstetric Complications
ANTEPARTUM BLEEDING
Maternal cardiovascular support is crucial to fetal
well-being. Chronic blood loss can lead to maternal
anemia and a related decrease in oxygen-carrying
capacity. Uncompensated acute bleeding results
in diminished blood volume, decreased systolic
pressure, decreased cardiac output, and ultimately
decreased placental perfusion. The net effect on the
fetus is decreased oxygenation and impaired nutrient delivery.
Gestational bleeding in the first or second
trimester of pregnancy has been linked to
increased risk of preterm labor, preterm birth,
PROM, and low birth weight.42 The most
common causes of hemorrhage late in pregnancy
include placental abruption and placenta previa. The
incidence of placental abruption is approximately
1%,19 and it is more common in older pregnant
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women.46 In an abruption, a normally implanted
placenta separates from the uterine wall before the
time of delivery, resulting in maternal bleeding and
a functional decrease in uteroplacental size. A relationship between hypertensive disorders, cocaine
use, and cigarette smoking and an increased incidence of abruptions has been reported.51 In those
with preterm rupture of membranes, the incidence
of placental abruption is 2% to 5%.14 In the presence of an intrauterine infection, the relative risk
increases ninefold. The separation may be partial or
complete, involving peripheral and/or central portions of the placenta. Fetal compromise relates to
the extent of the separation and to the frequent
need for preterm delivery. When the abruption
is small and bleeding is minimal, the pregnancy
may continue without significant fetal compromise;
however, remember that the decrease in uteroplacental surface area is irreversible and reduces the
absolute placental capability. As the fetus grows or
experiences additional stressors, its ability to tolerate
the abruption may change. Extensive abruptions are
poorly tolerated by both the fetus and mother; the
resulting maternal hemorrhage and decreased placental function lead to fetal asphyxia and, without
immediate intervention, to intrauterine demise.
A placenta previa exists when the placenta lies
abnormally low in the uterus and to some extent
covers or encroaches on the internal cervical os. In
the latter part of pregnancy, the normal elongation
of the lower uterine segment and changes in the
cervix disrupt the attachment of the overlying placenta. This generally presents as episodic, painless
maternal bleeding, often accompanied by preterm
labor. To avoid active labor with resulting maternal
hemorrhage, fetal lung maturity is assessed at 36 to
37 weeks.28 If the lungs are sufficiently mature, a
cesarean delivery is scheduled before the onset of
labor. Multiparity, maternal age, prior intrauterine
operations (≥3), and cigarette smoking are risk factors for placental previa.
46,63,133
Fetal compromise
relates to the extent of the previa, severity of
maternal hemorrhage, degree of the resulting
fetal hypoxia, degree of impaired fetal growth,
and gestational age at delivery.
51,130
Other placental abnormalities leading to antepartum bleeding include velamentous insertion and
vasa previa. A vasa previa occurs when naked fetal
vessels traverse the cervical os below the level of
the fetal presenting part; it is associated with a high
perinatal mortality rate. A velamentous insertion is
defined as the insertion of the umbilical cord into
the chorioamnionic membranes rather than the
mass of the placenta. These unprotected cord vessels have a higher rate of rupture. Rupture requires
emergency cesarean delivery to prevent fetal demise
and maternal hemorrhage. Antenatal diagnosis of
vasa previa and velamentous insertion with ultrasonography enables hospitalization in the third
trimester with planned delivery before the onset
of labor.
HYPERTENSIVE DISORDERS OF
PREGNANCY
31
Chronic hypertension in pregnancy, defined as hyper-
tension diagnosed before pregnancy or before 20
weeks of gestation, complicates 1% to 6% of births
in the United States each year. Chronic hyperten-
sion is associated with IUGR, preterm birth,
placental abruption, and stillbirth.51 The degree
of fetal compromise is related to the duration,
degree, and control of maternal hypertension.51
Women with chronic hypertension have a 25% risk
for developing superimposed preeclampsia.
51,135
Gestational hypertension was defined by the
Working Group on Research on Hypertension in
Pregnancy as hypertension arising after 20 weeks in
the absence of proteinuria.
135
Preeclampsia, a type of pregnancy-induced
hypertension, is a condition in which hypertension,
accompanied by proteinuria and edema, develops
during the second half of pregnancy in women with
or without preexisting hypertensive disease. It is
most common in primigravidae, obese women, and
women with multiple gestations and molar pregnancies, family history of preeclampsia, and history
of pregestational diabetes mellitus.51 As a perinatal
complication, preeclampsia is significant because
of its high toll in terms of both maternal and fetal
well-being.
Pregnancy is normally associated with vasodilation and decreased peripheral vascular resistance. The net effect is that, even though there is
a significant increase in blood volume, maternal
blood pressure does not increase during pregnancy. In contrast, pregnancy-induced hypertension is
associated with vasoconstriction and an increase
in peripheral vascular resistance and arterial pressure. The result is a reduction in blood flow to
the vital organs, including the kidney, liver, brain,
and uterus; reduced maternal blood volume; and
a host of maternal hepatic, CNS, and coagulation
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abnormalities. Associated fetal and neonatal risks
include IUGR, prematurity with all of its attendant problems, perinatal asphyxia, and perinatal
death. The risk to the infant increases with earlier
onset and increasingly severe maternal disease, such
as chronic hypertension with superimposed preeclampsia. Maternal seizures (eclampsia) further
compromise the fetus by promoting hypoxemia
and acidosis, which can result in intrauterine
demise.
HELLP syndrome, a severe form of pregnan-
cy-induced hypertension manifested by hemolysis,
elevated liver enzymes, low platelets, and renal
function abnormalities, carries a high risk for fetal
and maternal death. In many cases of HELLP syndrome, immediate delivery is indicated regardless of
the gestational age of the fetus.51 The use of steroids
in HELLP syndrome has been shown to improve
maternal oliguria, mean arterial pressure, mean
increase in platelet count, mean increase in urinary
output, and liver enzyme elevations. However, no
evidence suggests an improvement in maternal and
perinatal mortality or morbidity rates with the use
of maternal corticosteroids except with regard to
improvement in fetal lung maturity.
51
Drugs commonly used to treat pregnancy-induced hypertension include magnesium sulfate,
hydralazine, labetalol, nifedipine, and other antihypertensive agents. Magnesium sulfate is the most
commonly used agent in the United States for the
prevention of maternal seizures and has been shown
to be more effective than other regimens.
51
Hypotonia and CNS depression have been
reported as neonatal side effects, but magnesium therapy appears to be safe for the fetus.
150
Hypotonia and CNS depression are more likely
the result of coexisting complications, such
as prematurity and asphyxia. Hydralazine and
other antihypertensives are used in the treatment
of severe maternal hypertension; actions include
relaxation of the arterial bed, decreased vascular
resistance, and decreased blood pressure. Maternal
response to antihypertensives must be monitored
carefully, because precipitous decreases in blood
pressure reduce placental perfusion and further
compromise the fetus.
INFECTION
Group B streptococcus (GBS) is a major cause
of sepsis, meningitis, and death among newborn infants. It is estimated that 10% to 30% of
all pregnant women are colonized with GBS in
the vagina or rectum. The ACOG Committee on
Obstetric Practice now recommends “vaginal or
rectal group B streptococci screening cultures at 35
to 37 weeks of gestation for all pregnant women.”
Treatment for women with a positive culture, GBS
bacteriuria in the current pregnancy, or a previously
GBS-infected infant is usually penicillin.
PRETERM LABOR
6
Preterm birth, defined as any birth before 37
weeks of gestation, poses an unparalleled threat
to neonatal survival and well-being. In the
United States, 12% of all births are preterm,
and prematurity accounts for 70% of all neonatal deaths.15 Its cost, both human and economic, is
staggering, and its prevention is a primary focus of
modern obstetric care. Prevention is best accomplished through an aggressive effort to identify
women at risk and close follow-up to achieve early
recognition and appropriate intervention should
preterm labor occur. Unfortunately, many women
continue to receive inadequate prenatal care or
no care at all. Even women who obtain early and
ongoing care often fail to recognize the signs of
preterm labor and delay reporting symptoms until
intervention becomes difficult if not impossible.
Risk assessment markers in clinical use today
include an extensive review of obstetric, social, and
medical history.51 Measurements of cervical length
remain controversial. There are proponents of universal cervical length screening in those women
with no history of prior preterm birth. Applying
universal screening of cervical length presents the
difficulties of patient access and the potential for
unnecessary intervention. While the choice of
universal screening in a low-risk population is left
up to the discretion of the prenatal provider, if an
incidentally short cervix is noted at the time of the
second-trimester ultrasound examination, subsequent evaluation is necessary.
12
Fetal fibronectin is a glycoprotein secreted by
fetal membranes. Its presence in cervical-vaginal
secretions between 22 and 35 weeks of gestation has
been associated with an increased risk for preterm
labor and delivery. Its absence (high negative predictive value) can be used to identify patients who
are at low risk for preterm delivery. Cervical length
is assessed by three consecutive measurements using
transvaginal ultrasonography. The average length
of the cervix varies with gestational change but
51
CHAPTER 2 Prenatal Environment: Effect on Neonatal Outcome
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33
is approximately 4 cm in length from 26 weeks.
Length of cervix has been inversely correlated with
risk for preterm birth. Thus a combination of fetal
fibronectin and cervical length may be used to assess
the risk for preterm delivery for a given patient.
52
Depending on onset of short cervix in pregnancy, cervical cerclage, intramuscular progesterone (17-hydroxyprogesterone caproate), and vaginal
progesterone have been used to prevent preterm
labor with encouraging success.
29,142
A recent systematic review and meta-analysis of RCTs of vaginal versus intramuscular progesterone found that
daily vaginal progesterone, begun at 16 weeks of
gestation, is a reasonable, if not better alternative for
the prevention of recurrent spontaneous preterm,
singleton birth.
142
However, the quality of the
research data was evaluated as low or very low grade,
indicating that the true effect may be different from
the estimate of effect in the three RCTs included
in the meta-analysis.
142
More recent studies found
differing outcomes based on the types of progesterone used
not associated with an increase in GDM risk.
95,145
and that vaginal progesterone was
172
The Ohio Perinatal Quality Collaborative launched
a statewide initiative to reduce premature births by
10% by promoting progesterone prophylaxis and
achieved a 13% reduction in births before 32 weeks
in women with prior preterm birth.
85
Even though there has been some conflicting
evidence showing efficacy of intramuscular progesterone, it is still recommended for use in women
with risk factors for preterm birth.95 Evidence
supports the use of vaginal progesterone for women
with short cervix and no prior history of preterm
delivery and early cerclage with short cervix and
history of preterm delivery.
Although in many specific instances a definitive
cause cannot be identified, it is possible to identify
several factors that generally are associated with
preterm labor and delivery.12 When preterm labor
cannot be halted, it culminates in the delivery of
a physiologically immature infant. The result is
a host of neonatal problems that relate largely to
the degree of immaturity and also to compound-
ing problems, such as infant anomalies or maternal
disease, and to the events that led to the preterm
delivery (e.g., asphyxia resulting from a bleeding
placenta previa). Problems commonly encoun-
tered in preterm infants include respiratory
distress, asphyxia, hyperbilirubinemia, metabolic
disturbances, fluid and electrolyte imbalances,
neurologic and behavioral problems, infection,
nutritional deficits and feeding problems, ineffective thermoregulation, cardiovascular disturbances, chronic respiratory disease, and hematologic disturbances.
Beta-sympathomimetic agents are sometimes
used to prolong pregnancy in women having uterine contractions but no sign of infection. Mothers
may experience tachycardia and dysrhythmias,
hyperglycemia, hypokalemia, anxiety, nausea, and
vomiting. Myocardial ischemia and pulmonary
edema are rare but serious maternal side effects.
The fetus also may develop tachycardia and
hyperglycemia. Neonates born after beta-sym-
pathomimetic therapy may develop a rebound
hypoglycemia in response to in utero hyperglycemia and overproduction of insulin. Betasympathomimetic tocolytic agents increase
fetal aortic blood flow and fetal cardiac output
that might increase fetal systolic pressure and
cerebral blood flow, which can lead to an
increased incidence of intracranial bleeding in
immature fetal brains. More recent studies show
lower risk of side effects and improved prolongation of pregnancy from nifedipine compared with
beta-sympathomimetic tocolytics (see paragraph
on calcium channel blockers later).
87
Magnesium sulfate has also been employed as
a tocolytic. Magnesium sulfate decreases muscle
contractility, thereby inhibiting uterine activity and
effectively interrupting preterm labor. Neonatal
consequences of maternal magnesium administration include decreased muscle tone and
drowsiness, as well as decreases in serum calcium level.92 Serious maternal complications can
occur with concomitant usage of beta-adrenergic
receptor agonists or calcium channel blockers.12
Antenatal administration of magnesium sulfate for
neuroprotection of the preterm fetus, especially
related to gross motor function, is well estab-
55,58,146
lished.
Prostaglandins play an important role in the
onset of labor. Prostaglandin synthetase inhibitors,
such as indomethacin, are a class of pharmacologic agents that interfere with the body’s synthesis
of prostaglandin, thereby inhibiting prostaglandin-mediated uterine contractions. These drugs
have been used to treat preterm labor. They can
cause in utero constriction, or closure, of the
ductus arteriosus with resulting development of
fetal pulmonary hypertension and congestive heart
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failure. They also may lead to oligohydramnios
and must be used with caution, especially late
in the third trimester. Other neonatal risks
include decreased platelet activity and gastrointestinal irritation.92 Use of cyclooxygenase
(COX-2) inhibitors in preterm labor treatment is
being investigated.
100
Calcium channel blockers, such as nifedipine,
also have a demonstrated ability to interfere with
the labor process. Uterine contractility is directly
related to the presence of free calcium. Increased
calcium concentration enhances muscle contractility, whereas decreased calcium levels inhibit
contractility. Calcium antagonists block the entry
of calcium into cells and inhibit uterine muscle
contraction. In animal studies, these drugs have
been associated with fetal acidosis. However,
lower umbilical artery pH values or lower
Apgar scores have not been associated with
nifedipine.
92
Corticosteroid treatment of pregnant women
who are at sufficient risk to deliver prematurely
was first introduced in 1972 to enhance fetal lung
maturity. Human studies suggested possible benefits in reduction of the incidence and severity of
RDS and the incidence of patent ductus arteriosus.
Little or no evidence supported a reduction in
mortality rate or in the incidence of intraventricular hemorrhage, chronic lung disease, sepsis, necrotizing enterocolitis, or retinopathy of
prematurity with repeated antenatal corticosteroid therapy. Some of the suggested fetal risks
of repeated antenatal corticosteroid therapy
include decreased somatic and brain growth,
adrenal suppression, neonatal sepsis, chronic
lung disease, and death. All pregnant women
between 24 and 34 weeks of gestation who are at
risk for preterm delivery within 7 days should be
considered candidates for antenatal treatment with
a single course, such as 2 × 12 mg of betamethasone administered intramuscularly, within 24 hours.
Recent data have also shown that administration of
betamethasone in the late preterm period between
34 and 38 weeks of gestation is associated with
decreased neonatal respiratory complications.12
The evidence to date is clearly against the
routine administration of multiple antenatal
steroid courses.
16,134
The latest ACOG practice
bulletin recommends a single repeat course of
antenatal corticosteroids for women: (1) who
are less than
366
⁄7 weeks of gestation, (2) who
are at risk of preterm delivery within 7 days,
and (3) whose prior course of antenatal steroids
was more than 14 days previously.
16
ENVIRONMENTAL EFFECTS OF
LABOR ON THE FETUS
Effects of Contractions
During labor, the dynamics of uterine contractions
alter the intrauterine environment and influence the
fetus. A “healthy” fetus is equipped to withstand
the challenge of labor, but when the fetus is
compromised or the labor is dysfunctional, the
fetus can be taxed beyond its capacity, placing
it at risk for further compromise, asphyxia, or
intrauterine death.
Strong uterine contractions are characterized
by decreased blood flow through the intervillous
spaces in the placenta. As blood flow decreases, a
corresponding decline in placental gas exchange
occurs and the fetus must depend on its existing
reserves to maintain oxygenation until placental
blood flow is reestablished. The net effect is that
fetal Pao2 decreases as the consequence of uterine
contraction. In the fetus with adequate reserves,
the fall in Pao2 is not drastic; the fetus remains
adequately oxygenated and so can tolerate the
stress of labor.
Fetal Reserve
The factors that influence fetal reserves fall
into two general categories: those that diminish
reserves and those that exhaust reserves. When
fetal oxygen reserves are diminished, the fetus has
less-than-optimal oxygenation at the onset of a
contraction. This may occur as a consequence of
any condition that decreases placental exchange,
including reduced placental surface area caused
by abruption, placenta previa, an abnormally small
placenta, decreased placental perfusion caused by
maternal hypotension or hypertension, or maternal
hypoxemia. Oxygen reserves can be diminished also
as a result of a reduction in fetal oxygen-carrying
capacity, as in severe anemia or acute fetal hemor-
88
rhage.
A fetal reserve that is adequate at the onset
of labor can be exhausted by factors that place
unusual demands on the fetus. Exhaustion of
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reserves occurs with contractions that last for a
prolonged period, are of extremely high intensity,
or occur with increased frequency and without
an adequate recovery period between individual
contractions.88 This is often a consequence of
the use of oxytocic agents to induce or augment
labor.
Determination of cord gases at delivery provides objective evidence of the fetal metabolic
state at the time of birth.51 A base excess of
less than or equal to 12 mmol/L generally is
defined as the threshold that may be associated
with hypoxic injury.
124,137
Fetal pulse oximetry
may also be used. Decreased fetal pulse oximetry values, especially prolonged and recurrent
recordings less than 30%, are correlated with
abnormal fetal heart rate patterns, indicating
an association with fetal compromise and
metabolic acidosis.
153
However, a systematic
review found that the addition of fetal pulse
oximetry does not reduce and may increase
the caesarean delivery rate and that a better
method to assess fetal well-being in labor is
needed.
60
Fetal Response to ContractionInduced Hypoxia
When the fetal oxygen reserve is diminished or
exhausted, uterine contractions can precipitate
a significant fall in Pao2. The fetus is quite limit-
ed in its ability to compensate for this hypoxemia.
The adult mechanism, which involves increasing
total cardiac output by increasing heart rate, does
not play a major role in the fetal response. Instead,
the fetus responds with a redistribution of cardiac output as a means of maintaining critical
function; blood flow to the brain and heart
increases, whereas perfusion of less critical
organs is reduced.10 This mechanism enables
the fetus to survive brief episodes of hypoxia, but
severe and prolonged hypoxic episodes are poorly
tolerated.
Acute hypoxemia leads to the development
of acidosis and also produces a reflex bradycardia as a result of vagal stimulation, both of
which further compromise fetal oxygenation.
In addition, myocardial hypoxia has a direct
bradycardic effect.10 These mechanisms give
rise to one of the classic signs of fetal distress, the late deceleration, in which the peak
of uterine pressure, which also represents the
nadir of intervillous blood flow and the onset of
fetal hypoxemia, is followed by a decline in fetal
heart rate. Late decelerations are significant in that
they help identify the fetus who cannot tolerate
labor because of inadequate oxygen reserves and
they allow for the implementation of measures to
enhance fetal reserve, improve placental perfusion,
or interrupt labor.
168
Late decelerations are particularly ominous
when accompanied by loss of fetal heart rate
variability and/or fetal baseline tachycardia,
because these findings are indicative of fetal
acidosis. In the preterm infant, the findings of
decreased variability and tachycardia, with or without late decelerations, correlate highly with acidosis,
depression, and low Apgar scores.
168
Other Factors That Evoke a Fetal
Response During Labor
HEAD COMPRESSION
Pressure on the fetal head during labor, especially with pushing efforts in the second stage,
also produces a vagal response and a reflex
slowing of the fetal heart rate. In general, this
does not indicate hypoxia or fetal compromise and
often is seen in a healthy fetus. The deceleration
that accompanies head compression, also called
an early deceleration, is differentiated from the late
deceleration of fetal asphyxia by its timing in relation to a contraction. In early deceleration, the
heart rate begins to fall as a contraction builds,
reaching its lowest point as the contraction
peaks. As the contraction subsides, the heart
rate returns to baseline. The result is a uniformly shaped dip that mirrors the shape of the
contraction. In comparison, a late deceleration
also has a uniform shape but lags behind the
contraction, with the fall in heart rate beginning at or slightly after the contraction peak
and continuing to fall as the contraction subsides. With a late deceleration, the heart rate
does not return to baseline until well after the
contraction has ended.
CORD COMPRESSION
Compression of the umbilical cord occurs when
the cord is looped around fetal body parts, when
it is knotted or prolapses, or when amniotic fluid
is low (oligohydramnios). During labor, cord
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compression may be exacerbated by contractions
and descent of the fetus, resulting in varying
degrees of occlusion of the umbilical vessels
and diminution of blood flow. Partial venous
occlusion may be manifested by fetal heart rate
acceleration, whereas significant occlusion precipitates a rapid fall in heart rate, caused at least
in part by vagal reflex. Variable decelerations can
be spontaneous, occurring at any time, or
periodic, occurring with contractions. They
typically have an abrupt descent in heart rate
and may be V-, U-, or W- shaped—hence
the term variable deceleration. Periodic variable
decelerations are identified by a decline in heart
rate that generally begins before the contraction
peaks but, unlike early decelerations, falls rapidly
and does not mirror the shape of the contraction. Typically, recovery of the heart rate
also is rapid. However, when the occlusion is
severe or of long duration or if the fetus has
diminished oxygen reserves, recovery may be
slow, indicating fetal hypoxia and, in essence,
incorporating a component of late deceleration within the variable deceleration.
168
When variable decelerations are persistent and
worsening during labor in the presence of oligohydramnios, intrapartum amnioinfusions have
significantly decreased fetal heart rate abnormalities, acidemia at birth, and rates of cesarean
delivery.81 An amnioinfusion involves infusion of
fluid into the uterine cavity via an intrauterine
pressure catheter. This fluid provides cushioning
of the umbilical cord, which may reduce the
frequency and severity of the cord compression.
However, amnioinfusion is no longer standard
practice when moderate or thick meconium is
present.
MATERNAL PAIN MEDICATION
18,81
Maternal anesthesia and/or analgesia has the
potential to affect the infant, either during labor
and delivery or in the newborn period. The risk
is increased if the fetus is preterm or is otherwise
compromised. This is not to say that there is no
place for these drugs in obstetric care—only that
they must be used judiciously and with a clear
understanding of the risks and benefits involved.
Table 2.1 summarizes the effects of commonly
used analgesic and anesthetic agents on the fetus
and newborn.
18,127
TABLE
2.1
DRUG POSSIBLE FETAL AND NEONATAL SIDE EFFECTS
Narcotics Fetal and neonatal effects are related to the
Paracervical
block
Epidural and
spinal block
General
(inhalation)
anesthesia
CNS, Central nervous system.
FETAL AND NEONATAL EFFECTS OF
MATERNAL ANALGESIA AND ANESTHESIA DURING LABOR
dose, route, and timing of maternal administration and may be reversed by the administration
of a narcotic antagonist (naloxone):
• CNS depression
• Fetal bradycardia
• Depressed respiratory effort
• Decreased muscle tone and reflexes
• Decreased responsiveness
Fetal bradycardia and asphyxia related to
decreased uterine blood flow and direct fetal
myocardial depression
Fetal bradycardia and asphyxia related to
maternal hypotension
Fetal/neonatal toxicity
Neonatal respiratory depression after epidural
containing fentanyl
Fetal and newborn effects related to the duration
and depth of maternal anesthesia include the
following:
• CNS depression
• Respiratory depression
• Decreased responsiveness
ASSESSMENT OF FETAL
WELL-BEING
Over the past 30 years, the capability to assess fetal
well-being has advanced from simple auscultation of
the fetal heart to direct physiologic and biochemical
measurement of fetal status. With these advances, an
appreciation of the similarities between the fetus
and newborn, as well as a more complete understanding of the unique features of fetal life, has been
gained. This knowledge reinforces the importance
of viewing fetal physiology as a precursor of neonatal function and especially as a significant influence
on the success with which the fetus will complete
the adaptations required by the birth process.
The goal of antepartum fetal surveillance is to
answer the following questions: What is the safest
CHAPTER 2 Prenatal Environment: Effect on Neonatal Outcome
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37
environment for a fetus at the gestational age at
which the testing is taking place? Is the fetus more
likely to survive in utero for the week after testing,
or does the fetus have a significant risk for in utero
death based on the degree of environmental or
intrinsic intolerance demonstrated through testing? In the case of preterm infants, this may mean
delivery at a gestational age at which there is a high
likelihood for respiratory, neurologic, cardiac, gastrointestinal, and immunologic immaturity that will
require neonatal intensive care.
The obstetric practitioner has several tools available to help answer the preceding questions. First
and foremost is the identification of maternal conditions that may predispose the fetus to in utero
compromise. Examples of such conditions include
type 1 diabetes mellitus, chronic hypertension, collagen vascular disease, antiphospholipid antibody
disease, maternal cardiac or pulmonary disease, preeclampsia, blood group isoimmunization, in utero
infection, PROM, and maternal substance abuse.
This list is not all-inclusive but demonstrates several
commonly encountered conditions for which antepartum fetal surveillance is warranted.
Once the decision is made to assess fetal
well-being, four modalities are available in general practice to help the practitioner and patient
answer questions about the optimal environment
for the fetus at any given time—fetal movement counts, the contraction stress test (CST),
the NST, and the fetal biophysical profile.
Two additional tools often used by maternalfetal medicine specialists in certain clinical situations are Doppler flow studies and percutaneous
umbilical cord blood sampling (PUBS). None
of these tools is used as the sole determinant for
delivery; rather, each is used in conjunction with the
entire clinical picture. The choice of testing method
also is clinically driven; each method is useful in
certain clinical settings, but no one method is the
correct choice in all situations.
Although most of the procedures used to
monitor fetal well-being are decidedly high-tech,
the simple “kick count,” or fetal movement survey,
is a low-tech, low-cost screening tool. Many
women with an intrauterine fetal demise have
no identifiable risk factors that would place them
in a fetal testing protocol. Fetal motor activity
reflects the fetal condition in utero, and a
decrease in or absence of fetal movements
often presages fetal death. This is one reason
that many institutions ask their patients to begin
a fetal movement counting protocol at 26 to 32
weeks of gestation. Although there are continuing
study results, some centers have demonstrated
a significant decrease in the incidence of fetal
mortality rates after the institution of a fetal
movement counting protocol.
There are several different approaches to fetal
movement counting. None has been shown to be
superior.10 One approach is to have the patient
choose a certain time every day to rest in the
lateral position and count fetal movements. The
perception of 10 distinct fetal movements within 2 hours constitutes a reassuring session. The
most important aspect of this type of testing is to
emphasize to the patient the importance of notifying her practitioner immediately if the fetal movement counting has not met the established criteria.
A system must be in place in which patients have
immediate access to health care personnel 24
hours per day.
The CST is used in an attempt to evaluate
fetal response to uterine contractions.84 The
principle behind the CST is that uterine contractions cause a transient interruption in uteroplacental
perfusion. With normal fetal reserve, this intermittent interruption is well tolerated. With inadequate
or exhausted reserve, late fetal heart rate decelerations appear. Because late decelerations during labor
had been associated with fetal hypoxia and acidosis,
it was reasoned that similar interpretations could be
applied to contractions induced in the antepartum
patient. Thus the CST is considered a test of
uteroplacental reserve.
During a CST, uterine contraction activity is
evoked with either the use of maternal nipple stimulation or an intravenous infusion of oxytocin. The fetal
heart rate is charted using graph paper attached to a
monitor that uses a continuous wave ultrasound transducer placed on the maternal abdomen over the uterus. The minimum number of spontaneous or evoked
contractions necessary for adequate testing is three
contractions of 40 seconds’ duration in a 10-minute
period. The results are interpreted as follows:
• A negative CST result is one in which no late
fetal heart rate decelerations occur during the
examination.
• In a positive CST result, late decelerations occur
after 50% or more of the contractions, even if
contraction frequency is fewer than three in 10
minutes.
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• A suspicious or equivocal finding is one in which
intermittent late or significant variable decelerations occur.
• A CST result is considered unsatisfactory if fewer
than three contractions occur per 10 minutes or
a poor-quality tracing is obtained.
In many clinical situations, a positive CST
warrants delivery of the fetus because of
suspected in utero hypoxemia during periods of uterine contraction. However, there are
numerous exceptions to this rule. For example,
if a positive CST is noted in the presence of
maternal diabetic ketoacidosis, a correction of
the underlying metabolic process may reverse
the fetal acidosis and a negative CST may be
obtained subsequently. Thus the delivery of
a neonate who has metabolic acidosis and is
preterm can be avoided.
The NST is a tool used to indirectly assess
the integrity of the fetal autonomic nervous
system. The fetal heart is under the dual influ-
ences of the sympathetic and parasympathetic
nervous systems. By approximately 28 weeks of
gestation, 85% of fetuses demonstrate fetal heart
rate accelerations in response to fetal movement. Lack of these intermittent fetal heart rate
accelerations usually indicates a fetal sleep cycle.
However, many other intrinsic and extrinsic
factors, including fetal acidosis, may lead to an
absence of these intermittent accelerations in
heart rate. Examples include but are not limited to medication exposure, maternal smoking,
uteroplacental insufficiency, and fetal structural
or chromosomal anomalies. Factors leading to
maternal acidosis (severe anemia, congenital heart
disease, and sepsis) also can result in fetal acidosis
and nonreactive NST.
The NST is performed with the patient in a
semi-Fowler’s or lateral tilt position. As in the CST,
the fetal heart rate is monitored with an external
transducer. NSTs are interpreted as either reactive
or nonreactive. An accepted definition of a reactive
NST is an increase in fetal heart rate of 15 beats/
min for 15 seconds above the baseline heart rate
occurring twice in a 20-minute period.10 A nonreactive NST is defined as lacking the necessary fetal
heart rate accelerations during a 40-minute period.
The following may be candidates for nonstress
testing:
• Women who have diabetes that must be con-
trolled with medication
• Women who have pregnancy-induced hyperten-
sion, preeclampsia, or intrinsic renal disease
• Women in whom fetal IUGR, oligohydramnios,
or postdate pregnancy has been determined
• Women who have reported decreased fetal
movement
The NST has certain advantages over the CST. It
does not entail the production of uterine contractions, and so there are fewer potential problems or
contraindications to the NST. Because the NST is
quicker and easier to conduct, it is often the firstline screening test of fetal well-being. Its disadvantages are that it does not evaluate uteroplacental
reserve and that it has a higher false-positive rate
than the CST.
When the NST is nonreactive, an option that
is often used in lieu of the CST or delivery of the
fetus is the biophysical profile (BPP) (Table 2.2). This
test combines the NST with real-time ultrasound
TABLE
2.2
BIOPHYSICAL VARIABLE NORMAL (2) ABNORMAL (0)
Fetal breathing—At least one episode of at least 30 seconds during a 30-minute observation Present Absent
Gross body movement—At least three body or limb movements during a 30-minute observation ≥3 ≤2
Fetal tone—One episode of extension or flexion of limbs or trunk during a 30-minute observation Present Absent
Reactive nonstress test—At least two episodes of 15 beats/min fetal heart rate accelerations during
30-minute observation
Amniotic fluid volume—A pocket of fluid that measures at least 2 cm in two planes perpendicular to
each other (2 × 2–cm pocket)
Normal Score: 8–10
BIOPHYSICAL PROFILE SCORING
Yes No
Present Absent
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