Abstract
The assessment of fetal well-being is a critical tool in ensuring optimal neonatal outcomes from both pregnancy and labor. This is particularly relevant for the recognition of the infant that may be at risk of hypoxic-ischemic cerebral injury. The identification of an intrauterine disturbance in gas exchange between the human fetus and mother (i.e., asphyxia) or the likelihood that such a disturbance will occur during labor or delivery is critical to improving the neurological outcomes for all infants, particularly those at greatest risk such as the growth-restricted infant. Moreover, attempts at prevention of the brain injury caused by intrauterine asphyxia, antepartum and intrapartum, demand precise awareness of when such injury is imminent. Although the most definitive information concerning the detection of hypoxic-ischemic insult to the fetus still applies primarily to the intrapartum period, major advances in antepartum assessment have been made. Thus, this chapter reviews the major current means of antepartum assessment of the fetus and then the approach to intrapartum assessment. In addition, we briefly summarize novel fetal and placental imaging techniques using magnetic resonance imaging.
Keywords
Fetal assessment, intrapartum assessment, electronic heart monitoring, fetal ultrasound, fetal well-being
The focus in this chapter is the assessment of fetal well-being, particularly as a means for recognition of the infant that may be at risk of hypoxic-ischemic cerebral injury. The identification of an intrauterine disturbance in gas exchange between the human fetus and mother (i.e., asphyxia), or the likelihood that such a disturbance will occur during labor or delivery is critical in view of the large body of data that intrauterine asphyxia occurs in a large proportion of infants with hypoxic-ischemic encephalopathy. Moreover, attempts at prevention of the brain injury caused by intrauterine asphyxia—antepartum and intrapartum—demand precise awareness of when such injury is imminent. Although the most definitive information concerning detection of hypoxic-ischemic insult to the fetus still applies primarily to the intrapartum period, major advances in antepartum assessment have been made. This chapter reviews the major current means of antepartum assessment of the fetus and the approach to intrapartum assessment. In addition, we will briefly summarize novel fetal and placental imaging techniques using magnetic resonance imaging (MRI). Issues related to genetic disorders and cerebral genesis (Unit 1) and fetal cerebral metabolic disorders ( Chapter 27 , Chapter 28 , Chapter 29 ) are reviewed in other sections of the book.
Antepartum Assessment
Although the nature, timing, and frequency are not entirely established, it is clear that some hypoxic-ischemic insults affect the brain before labor and delivery (i.e., during the antepartum period). The search for means of assessing such disturbances, acute or chronic, has been the subject of a vast amount of obstetrical research. Antepartum surveillance regimens were developed principally to prevent stillbirth. Thus, the evaluation of antepartum techniques of monitoring for a reduction in hypoxic-ischemic injury has not been specifically studied. However, with the expansion of monitoring, the impact of monitoring on Apgar scores and neonatal intensive care admission has allowed some insights (see later). In this section, a brief review of the current means of fetus evaluation during the antepartum period is provided. The techniques are described as those based on measurement of fetal movement, fetal heart rate, a combination of factors that include fetal movement and heart rate (biophysical profile), fetal growth, and blood flow velocity in uterine and fetal blood vessels ( Table 17.1 ). All of these techniques are usually applied with greater frequency to women who are deemed to be at greater risk for pregnancy and neonatal complications. Thus, identifying the fetus at risk for cerebral injury may allow timely detection of impending fetal jeopardy allowing intervention or delivery to reduce the risk of possible cerebral injury. Pregnancy conditions that have been associated with increased risk of short-term and long-term neurological sequelae for which antenatal testing may be appropriate are outlined in Table 17.2 .
| Fetal movement |
| Detection by maternal perception or by real-time ultrasonography |
| Fetal heart rate |
| Nonstress test : response of fetal heart rate to movement |
| Contraction stress test : response of fetal heart rate to stimulated (oxytocin and nipple stimulation) or spontaneous uterine contraction |
| Fetal biophysical profile |
| Combination of fetal breathing, movement, tone, heart rate reactivity, and amniotic fluid volume |
| Fetal growth |
| Detection of intrauterine growth retardation |
| Fetal blood flow velocity |
| Detection by the Doppler technique of flow velocity in umbilical and fetal systemic and cerebral vessels |
| Maternal conditions |
|
| Fetoplacental conditions |
| Fetal growth restriction |
|
| Other |
| Environmental risk—ionizing radiation, lead, mercury |
A common theme found in relation to all the techniques outlined later is that the presence of normal results is associated with good fetal and neonatal outcomes. Thus, the absence of any abnormality can be reassuring . However, abnormal tests have low positive predictive values for abnormal outcomes, making their utility as diagnostic tests for fetal vulnerability poor. Finally, many studies have not included outcomes of greatest relevance, including neonatal morbidity and neurodevelopmental outcomes.
Fetal Movement and Behavioral States
Fetal movement is a useful indicator of fetal health. Techniques for monitoring fetal movement have included systematic maternal recording of perceived activity (the most convenient and widely used), electromechanical devices (tocodynamometry, primarily an investigative tool), and real-time ultrasonography (see Table 17.1 ). Real-time ultrasonography has received increasingly wide clinical and investigational use because of the diversity of information that it can provide.
Fetal movements are one aspect of the determination of fetal behavioral states. Fetal behavioral states are defined according to the quantitative and qualitative aspects of fetal body movements, eye movements, and fetal heart rate. Distinct fetal states are definable by 36 to 38 weeks of gestation and recognizable behavioral states at that time are summarized in Table 17.3 . These states approximate neonatal behavioral states, that is, quiet sleep (1F), REM sleep (2F), quiet waking (3F), and active waking (4F). Active sleep (2F) is the most frequently observed, followed by quiet sleep (1F). The waking states are either infrequent (4F) or rare (3F).
| STATE a | BODY MOVEMENTS | EYE MOVEMENTS | FETAL HEART RATE PATTERN |
|---|---|---|---|
| 1F | Absent (occasional startle) | Absent | Narrow variability, isolated acceleration |
| 2F | Present (frequent bursts) | Present | Wide variability, acceleration with movement |
| 3F | Absent | Present | Wide variability, no accelerations |
| 4F | Present (almost continuous) | Present (continuous) | Long accelerations or sustained tachycardia |
a These fetal states approximate neonatal behavioral states, that is, quiet sleep (1F), active sleep (2F), quiet waking (3F), and active waking (4F).
Maturational Changes
Distinct maturational changes in fetal movement can be identified ( Fig. 17.1 ). Although with ultrasonography it is possible to detect movement as early as the second month of gestation, maternal perception of movement ( quickening ) occurs at approximately 16 weeks. Thereafter, the movements increase in strength and reach a plateau from 26 to 32 weeks of gestation. An abrupt fall to a second plateau occurs between 32 and 36 weeks. No appreciable change occurs thereafter until delivery.
Prechtl and others emphasized the quality of fetal movements and the striking maturational changes in the variety and complexity of these movements. Certain fetal movements increase in incidence gradually with advancing gestation (e.g., breathing, sucking, and swallowing), other movements increase in incidence to a plateau (e.g., general movements, isolated arm movements), and still others increase in incidence and then decrease (e.g., startles, hiccups).
Relation to Fetal Well-Being
The relation of quantity and quality of fetal movement to fetal well-being is illustrated by the study summarized in Fig. 17.2 . Decreased fetal movements perceived by the mother over the 7 days before delivery can be documented in a series of pregnancies with “unfavorable perinatal outcome” (i.e., abnormal intrapartum fetal heart rate patterns, depressed Apgar scores, and antepartum or intrapartum stillbirth). The most common denominator of fetal inactivity was chronic uteroplacental insufficiency. A report that suggests the value for prompt detection and evaluation of decreased fetal movement involved pregnant women who were instructed to report to the delivery unit if 2 hours elapsed without 10 fetal movements perceived. Further evaluations and any indicated interventions for fetal compromise were performed. During the study period, fetal mortality among women with such decreased fetal movement was 10 per 1000; in the control period immediately before onset of the study, fetal mortality with such decreased fetal movement was 44 per 1000.
A recent Cochrane review of the efficacy of fetal movement counting for the assessment of fetal well-being included five studies with 71,458 women. All included women with uncomplicated pregnancies, except one study which included high-risk women as participants. Two studies compared fetal movement counting with standard care, as defined by trial author. Two studies compared two types of fetal movement counting: comparing once-a-day (Cardiff count-to-10) with more than once-a-day fetal movement counting methods. One study compared fetal movement counting with hormone assessment evaluated with an average of five determinations of serum total estriol and human placental lactogen.
The first comparison of fetal movement monitoring compared with standard care showed no difference in mean stillbirth rates (standard mean difference [SMD] 0.23, 95% CI –0.61 to 1.07) or fetal deaths. There was no difference in cesarean section rate between groups within any of these three comparisons of fetal movement monitoring. There were no data on perinatal mortality or severe morbidities.
The conclusions of the Cochrane review were that sufficient evidence did not exist to influence clinical practice. In particular, only two studies compared the counting of fetal movements with standard antenatal care. It is noteworthy that the larger cluster randomized controlled trial (RCT) comparing routine fetal movement counting with normal care , which included fetal movement counting at the discretion of the caregiver (8.9% in a subset of control participants), demonstrated a strong trend to a reduction in stillbirth. However, this did not translate to reduced perinatal mortality or morbidity across all studies, including this RCT.
Fetal Neurological Examination
The observations described in the preceding sections are reminiscent of those made during the neonatal neurological examination. The utilization of fetal movements as part of a detailed analysis of fetal behavior by real-time ultrasonography led to the identification of distinct behavioral states , as noted earlier. These analyses include assessment of a variety of specific body movements (e.g., yawning, stretching, and startle), as well as fetal eye movements, posture, breathing, and heart rate. The analogy of these phenomena to those observed after birth in the premature infant (see Chapter 9 ) is obvious, and, to a major extent, one can consider these observations a kind of fetal neurological examination . When amplified by such assessments as habituation of the fetus to vibrotactile stimuli or response to acoustical stimuli, the analogy to neurological assessment becomes even more impressive. Detailed analysis of the quantity and quality of fetal breathing can provide still further information about the fetal nervous system. a
a References .
With the wide use of real-time ultrasonography, standardization of observable neurological phenomena, and, importantly, the correlation of aberrations with the topography of neuropathology, highly valuable evaluation of the fetal central nervous system and dysfunction should be possible. The design of appropriate interventions for disturbances then would be an appropriate next step.Fetal Heart Rate: Nonstress and Stress Tests
The evaluation of fetal well-being by antepartum fetal heart rate testing is a standard obstetrical practice in high-risk pregnancies. The two commonly used techniques determine fetal heart rate changes with either stimulated (or spontaneous) uterine contractions (contraction stress test) or spontaneous fetal events (e.g., fetal movement test, or nonstress test) (see Table 17.1 ).
Nonstress Test
Of the two techniques, the nonstress test is the approach used as an initial evaluation. In general, the particular value of the technique is the determination of a healthy fetus based on demonstration of at least two accelerations of fetal heart rate during the period of observation (usually ≈40 minutes), generally in association with fetal movement or vibroacoustical stimulation. The accelerations must exceed 15 beats/min and last at least 15 seconds; the normal result is called a reactive nonstress test. A nonreactive test is characterized by the failure to note such accelerations over the observation period. The demonstration of accelerations of fetal heart rate with acoustical stimulation and the correlation of a reactive acoustical stimulation test with the conventional nonstress test have led to use of such stimulation as part of the nonstress test in many centers.
In the predictive value of nonstress testing, the incidence of fetal distress leading to cesarean delivery increases from about 1% to 20% when antepartum reactive and nonreactive patterns are compared. It is clear, however, that most abnormal or nonreactive tests are not followed by difficulties with labor and delivery. A normal, reactive nonstress test is highly predictive of fetal well-being. Thus, as with most other modes of fetal evaluation including antepartum and intrapartum, the prediction of a normal fetus and the relative lack of need for intervention are the greatest values of the test . However, the test does not detect such important maternal-fetal problems as oligohydramnios, umbilical cord or placental abnormalities, growth disorders, and twin demise. When suspicion or concern for such problems exists, another approach using ultrasonography, as in fetal biophysical profile, is essential. Despite the rational approach to these measures of fetal behavior and well-being, several randomized prospective trials that have used weekly nonstress surveillance tests have shown no benefit to the fetus or infant.
Contraction Stress Test
The contraction stress test was most commonly used in the past as a follow-up evaluation after a nonreactive stress test. Experimental data suggest that the occurrence of late decelerations with contractions, the basis for a positive (abnormal) stress test , is an early warning sign of uteroplacental insufficiency. The established clinical and experimental premise of the stress test is that chronic uteroplacental insufficiency results in late decelerations of the fetal heart rate, a sign of fetal hypoxia (see following discussion) in response to uterine contractions; these can be stimulated by breast stimulation or oxytocin infusion. In approximately 10% of women, spontaneous uterine contractions obviate the need to stimulate uterine contractions. A positive (abnormal) result is indicated by persistent late decelerations over several or more contractions; these positive tests can be subdivided further as reactive , when accompanied by accelerations at some time during the test, or nonreactive , when not accompanied by accelerations. An equivocal result refers to the occurrence of nonpersistent late decelerations . A negative stress test is defined as absence of any late decelerations with the contractions.
As with nonstress testing and other fetal assessments, a negative stress test is a reliable indicator of fetal well-being. The predictive value of a positive stress test was demonstrated in one multi-institutional study of high-risk pregnancies. A negative test was followed by perinatal death in less than 1% of cases versus 5% to 20% of infants with positive contraction tests. The lower value was for infants with reactive positive tests; the higher value was for those with nonreactive positive tests. Similarly, an Australian study showed that among 72 patients with nonreactive positive spontaneous contraction stress test results, there was a 28% perinatal mortality rate. Of the 52 infants who survived the neonatal period, 42 were assessed with 27% having neurological handicap.
Currently, the contraction stress test is no longer the principal method for follow-up in most centers. This change relates to logistical and interpretive difficulties and relatively low positive-predictive values. The fetal biophysical profile is now favored as the primary means of fetal surveillance for high-risk pregnancies, identified by a nonreactive nonstress test or other evidence.
Fetal Biophysical Profile
In view of the relatively high incidence of false-positive assessments with the tests of fetal heart rate just described, a series of fetal measures , termed a composite biophysical profile , has been used to refine antepartum evaluation. These measures include quantitation not only of fetal heart rate reactivity (see the earlier discussion of the nonstress test), but also of fetal breathing movements , gross body movements , fetal tone (as assessed by posture and flexor-extensor movements), and amniotic fluid volume (see Table 17.1 ). Each item is graded, usually on a score of 0 to 2. The use of real-time ultrasonography has made such an assessment possible, and the relative ease of this methodology in modern obstetrical centers has led to widespread use. The rationale of using such a profile is entirely reasonable (i.e., the various measures reflect activity of several levels of the central nervous system, including cerebrum, diencephalon, and brain stem). The predictive value of the score is demonstrated by the data in Fig. 17.3 , which illustrate the relation of the fetal biophysical score to umbilical venous pH determined by cordocentesis. Similar correlations are available regarding incidence of meconium passage during labor, signs of intrapartum fetal distress, and perinatal mortality. Of particular importance, the degree of abnormality of the fetal biophysical score has been shown to correlate with cerebral palsy ( Fig. 17.4 ) and predicted perinatal mortality ( Table 17.4 ). Data from a single center suggested that alterations in obstetrical management provoked by the results of the score could lead to a threefold to fourfold decline in cerebral palsy rates. Despite these positive results, a recent Cochrane review found no significant difference in outcomes between those high-risk pregnancies monitored with biophysical profile as compared with other forms of fetal assessment, mainly fetal heart rate monitoring. This supports the challenge in the widespread implementation of these evaluative tools of fetal well-being in randomized controlled trials, despite strong and rational observational data. The apparent lack of benefit may relate to subject selection, application of the testing, and/or limitations in the outcome measures.
| BIOPHYSICAL PROFILE SCORE a | INTERPRETATION | PREDICTED PERINATAL MORTALITY | RECOMMENDED MANAGEMENT |
|---|---|---|---|
| 0/10 | Severe acute asphyxia | 60/100 | Immediate delivery by cesarean section |
| 2/10 | Acute fetal asphyxia, most likely with chronic decompensation | 125/100 | Delivery for fetal indications (usually cesarean section) |
| 4/10 | Acute fetal asphyxia likely; if oligohydramnios present, chronic asphyxia also very likely | 9.1/100 | Delivery by obstetrically appropriate method with continuous monitoring |
| 10/10 | No evidence of fetal asphyxia | <0.1/100 | No acute intervention |
Fetal Growth
As with other antepartum assessments, advances in ultrasound technology have provided the capability of accurate quantitative assessment of fetal growth. The particular value of this assessment is in the detection of intrauterine growth retardation (see Table 17.1 ), although other aberrations of growth (e.g., large body size and large head) have important implications for management of labor, delivery, and the neonatal period, as discussed elsewhere in this book. Detection of intrauterine growth retardation is important, principally because significant management decisions follow. Most such fetuses are “constitutionally small,” are not at increased perinatal risk, and do not require aggressive intervention. However, some such infants (≈5% to 10%) exhibit a major developmental anomaly, including chromosomal aberration, that may require further intrauterine assessment (e.g., amniocentesis and chromosomal or other genetic analyses). Of greatest importance, particularly in this context, is that approximately 10% to 15% of infants with intrauterine growth retardation are growth retarded because of uteroplacental failure and are at risk for intrapartum asphyxia . In one series from a single high-risk service, 35% of growth-retarded fetuses exhibited intrapartum fetal heart rate abnormalities indicative of fetal distress. A significant increase in fetal asphyxia, as judged by cord acid-base studies, was apparent even when growth-retarded infants were compared with other high-risk groups. Moreover, growth-retarded infants with intrapartum fetal heart decelerations demonstrate considerably higher umbilical artery lactate levels than do normally grown infants with similar decelerations. Hence, growth-retarded infants tolerate labor less well than do normally grown infants, perhaps in part due to deficient stores of glycogen in liver, heart, and, possibly, in the brain. Therefore, antepartum detection of such infants is important in formulating rational decisions concerning further assessment of the fetus (e.g., fetal biophysical profile, Doppler blood flow velocity studies) and optimal management of labor and delivery (see next section).
Doppler Measurements of Blood Flow Velocity in Maternal Umbilical and Fetal Cerebral and Ductus Venosus Vessels
Doppler velocimetry is now a well-described technique used to assess fetal status ( Table 17.5 ). Several vessels have been interrogated, including the (maternal) uterine artery, fetal middle cerebral artery (MCA), umbilical artery, umbilical vein, and ductus venosus (DV). The most commonly examined and clinically useful vessel is the fetal umbilical artery. The waveform in normally growing fetuses is characterized by high- velocity diastolic flow; the commonly measured indices include systolic/diastolic ratio, resistance index, and pulsatility index (PI) (see Chapter 10 ). Marked abnormality in the waveform is characterized by absent or reversed diastolic flow. These waveforms correlate histopathologically with small artery obliteration in placental tertiary villi, and functionally with fetal hypoxia, acidosis, and prenatal morbidity and mortality. These studies have been undertaken predominantly in women who have a fetal diagnosis of intrauterine growth retardation.
| METHOD | MEASURES | INDICATIONS | VALUE |
|---|---|---|---|
| Umbilical cord artery | Pulsatility index | High-risk fetus, particularly IUGR | Reduction in fetal mortality and in obstetrical interventions |
| Resistive index | |||
| Diastolic flow—absent or reversed | |||
| Fetal middle cerebral artery | Cerebral blood flow velocity | High-risk fetus, particularly IUGR | Abnormal MCA PI was associated with greater perinatal morbidity |
| Resistive index | |||
| Pulsatility index | |||
| Fetal ductus venosus | a-Wave characteristics | IUGR—particularly useful between 20 and 32 weeks gestation | Determination of delivery by DV measures resulted in slight increase in mortality but reduction in morbidity |
| Diastolic flow measures |
Umbilical Artery
Most studies based on the use of Doppler in pregnancy have focused on the umbilical artery. a
a References .
The principal quantitative parameters of the Doppler waveform used have been the pulsatility index of Gosling (peak systolic velocity [S] − end diastolic velocity [D]/mean velocity), the resistance index of Pourcelot (S − D/S), and the S/D ratio . The values of these ratios, in general, are not affected by the angle of insonation, which is clearly difficult to maintain as a constant in the clinical situation. The pulsatility index and the resistance index reflect vascular resistance, in large part. The principal change in umbilical artery blood flow velocity with progression of normal pregnancy is a decline in the resistance parameters. Although the decline is gradual, a more pronounced decrease occurs after 30 weeks of gestation. This decrease is considered secondary to a decrease in placental vascular resistance, related particularly to increased numbers of small vessels. A similar phenomenon was documented in the fetal lamb. The decrease in placental vascular resistance with advancing pregnancy is accompanied by an increase in volemic placental blood flow, calculated in human fetuses by simultaneous measurements of the blood flow velocity in the umbilical vein and the cross-sectional area of that vessel by combined Doppler and imaging ultrasonography ( Fig. 17.5 ).
The major application of Doppler studies of blood flow velocity in the umbilical artery has been in the investigation of the high-risk fetus. a
a References .
In intrauterine growth retardation, the principal finding is an increase in the resistance measures. aa References .
With progression of this disturbance in resistance measures in the umbilical artery, marked impairment of the end diastolic flow or even loss or reversal of diastolic flow (an ominous sign) may occur ( Fig. 17.6 ).
In one study, the changes in resistance indices preceded antepartum late heart-rate decelerations in more than 90% of fetuses who developed such decelerations, and the median duration of the interval between the severe abnormality of resistance measure and decelerations was 17 days. The importance of the rising placental vascular resistance to the fetus is shown by the striking curvilinear relationship between the pulsatility index in the umbilical artery and the lactate concentration in fetal blood, a measure of fetal hypoxia ( Fig. 17.7 ). The clinical predictive value of the diastolic flow in the umbilical artery was apparent in a study of 459 high-risk pregnancies. Thus, the rate of fetal or neonatal death in the presence of end diastolic flow was 4%, increased to 41% with absence of flow, and increased to 75% with reversal of flow. With further prompt and detailed fetal assessments and appropriate interventions, an unfavorable outlook with absence of diastolic flow has not been so evident. However, reversal of flow is associated with a considerable risk of fetal compromise, perinatal mortality, neonatal neurological disturbances, and subsequent neurodevelopmental disability, with the risk magnitude varying considerably with the selection of the population studied.
The use of Doppler assessment of the umbilical artery flow in fetuses with growth restriction or those at risk (e.g., hypertensive pregnancies) has been shown to lead to a reduction in perinatal mortality and reduced unnecessary obstetrical intervention. Further meta-analyses, comparing the use of umbilical Doppler in high-risk groups, have confirmed this conclusion. A recent Cochrane review with 18 studies and >10,000 pregnancies demonstrated that women with Doppler assessment had a significantly lower perinatal mortality (1.2%) compared with those without Doppler studies (1.7%) (RR: 0.67; 95% CI: 0.46, 0.96). Although the data for secondary outcomes showed that there were fewer adverse outcomes in the Doppler group, this finding did not reach statistical significance. Interestingly, there was a reduction in interventions such as induction of labor and cesarean delivery in the Doppler group. Importantly, though, there is a lack of data on long-term neurological development on the infants in either group, and whereas the quality of data is described as low, the most recent study suitable for inclusion is more than a decade old.
The central abnormality in the growth-retarded fetus leading to the increase in placental vascular resistance is a disturbance in placental vessels. The major features include loss of small blood vessels, decreased vascular diameter because of media and intima thickening, and thrombosis. Placental vascular obstruction produced by a variety of experimental techniques in pregnant sheep reproduced the changes in the resistance measures observed in the human fetus. Indeed, elevated umbilical artery resistance measures have been observed in a variety of pathological conditions of the placenta, including partial abruption, placental scarring from intervillous thrombosis, and inflammatory villitis secondary to bacterial or viral infection. Accordingly, the value of this technique in the evaluation of a wide variety of high-risk pregnancies is very high.
The utility of Doppler umbilical arterial evaluation was recently recognized by the Society for Maternal-Fetal Medicine, which published a clinical guideline concerning Doppler assessment in intrauterine growth restriction (IUGR) . The recommendations included: (1) Doppler examination of any vessel is not recommended as a screening tool for identifying pregnancies that will subsequently be complicated by IUGR; (2) antepartum surveillance of a viable fetus with suspected IUGR should include Doppler examination of the umbilical artery, as its use is associated with a significant decrease in perinatal mortality; (3) once IUGR is suspected, umbilical artery Doppler studies should be performed usually every 1 to 2 weeks to assess for deterioriation, and, if normal, they can be extended to less frequent intervals; (4) Doppler assessment of additional fetal vessels has not been sufficiently evaluated in randomized trials to recommend its routine use in clinical practice in fetuses with suspected IUGR; (5) antenatal corticosteroids should be administered if absent or reversed end-diastolic flow is noted before 34 weeks in a pregnancy with suspected IUGR; (6) as long as fetal surveillance remains reassuring, women with suspected IUGR and absent umbilical artery end-diastolic flow may be managed expectantly until delivery at 34 weeks; and (7) as long as fetal surveillance remains reassuring, women with suspected IUGR and reversed umbilical artery end-diastolic flow may be managed expectantly until delivery at 32 weeks.
In contrast, Doppler measurement of umbilical artery flow has been shown repeatedly not to be useful in a low-risk or unselected population. A recent Cochrane review, including >14,000 women from 20 studies, compared the outcomes of low-risk pregnancies with either routine ultrasound or no Doppler ultrasound. This comparison failed to demonstrate a reduction in perinatal death or serious neonatal morbidity in the Doppler group, nor were there differences in the secondary outcomes, including prematurity, mode of delivery, neonatal resuscitation, or a 5-minute Apgar score <7.
Fetal Cerebral Vessels
Soon after the initial applications of Doppler for study of umbilical blood flow velocity followed the successful study of blood flow velocity in fetal cerebral vessels, particularly the MCA. This now widely used methodology allows monitoring during pregnancy of cerebral hemodynamics, perhaps the most crucial physiological process with regard to fetal brain injury.
During normal pregnancy, in contrast to the decreasing values for resistance measures defined in the umbilical circulation, values in the cerebral circulation change little until approximately the last 5 weeks, when a distinct decline is apparent ( Fig. 17.8 ). In addition, mean cerebral blood flow velocity has been shown to increase during the same period that resistance appears to decrease. This combination of findings suggests an increase in cerebral blood flow during the last trimester of pregnancy, perhaps related to cerebral vasodilation, or development of vascular beds, or both. A particular role for development of cerebrovascular reactivity to relatively low oxygen tension in the fetus is suggested by the findings that cerebral resistance indices in the fetus have been shown to be more responsive to blood oxygen tension than to carbon dioxide tension, and that in the immediate postnatal period, when blood oxygen tensions rise dramatically, cerebral mean flow velocity transiently declines markedly (consistent with an increase in cerebrovascular resistance).
As with Doppler studies of the umbilical vessels, study of cerebral blood flow velocity has been routinely directed at the growth-retarded fetus. The dominant abnormality has been a diminished value of cerebral resistance indices, in contrast to the elevated value in the umbilical artery ( Fig. 17.9 ). a
a References .
This apparent vasodilation in the cerebrum at a time of decreasing umbilical flow has been interpreted as an adaptive response, perhaps mediated by hypoxia, and has been termed fetal brain sparing . It seems reasonable to suggest that, with severe impairment of umbilical flow and hypoxia, such an adaptive response could become insufficient. Indeed, the decline in cerebral resistance indices and the increase in umbilical resistance indices have been quantitatively combined as a cerebral-to-umbilical ratio. This ratio has been predictive of such subsequent disturbances as fetal distress requiring cesarean section, fetal acidosis, and early neonatal complications ( Table 17.6 ).
| RATIO <1.08 ( n = 18) a | RATIO >1.08 ( n = 72) a | |
|---|---|---|
| Small for gestational age | 100% | 38% |
| Cesarean section (for fetal distress) | 89% | 12% |
| Umbilical vein pH (mean) | 7.25 | 7.33 |
| Five-minute Apgar score <7 | 17% | 3% |
| Neonatal complications b | 33% | 1% |
a Ratio of pulsatility index from cerebral circulation to index from umbilical artery; normal mean value is approximately 2.0.
b Intracerebral hemorrhage, seizures, respiratory distress syndrome.
The value of MCA Doppler in the prediction of adverse fetal outcome and fetal assessment has been inconsistent. Some studies have suggested that the MCA Doppler measures are useful, whereas others have found poor predictive value.
Recently, a meta-analysis of 35 eligible studies including 4025 fetuses was performed. It is worth noting that within the included studies the definition of IUGR varied, the timing of MCA recordings in relation to outcomes differed, and the definition of abnormal MCA also varied, though most used PI < 2 SD or PI < fifth centile. This meta-analysis found that low MCA PI appears to be predictive of impaired fetal well-being assessed either by acidosis (pH < 7.20) at birth or by higher likelihood of 5-minute Apgar score <7 (positive LR: 1.65 [1.07, 2.52]), and increased admission to a NICU (positive LR: 4.00 [2.16, 7.50], negative LR: 0.62 [0.47, 0.82]). Abnormal MCA recording was also predictive of an overall composite measure of adverse perinatal outcome (positive LR: 2.77 [1.93, 3.96], negative LR 0.58 [0.44, 0.69]) and perinatal mortality (positive LR: 1.36 [1.10, 1.67], negative LR: 0.51 [0.29, 0.89]). Although these findings suggest that there is an association between abnormal MCA recordings and adverse outcomes, the association is weak.
Finally, the potential value of Doppler study of the cerebral circulation in other fetal states is suggested by the demonstration of increased values for pulsatility index in the presence of hydrocephalus. This observation is identical to that made postnatally with posthemorrhagic hydrocephalus (see Chapters 10 and 24 ), and it raises the possibility of the use of Doppler in determination of the need for intervention in fetal hydrocephalus. Changes in cerebral blood flow velocity also have been documented with changes in fetal behavioral states and after administration of indomethacin to the mother.
Ductus Venosus
The DV is a fetal vessel connecting the abdominal umbilical vein to the left portion of the inferior vena cava just below the diaphragm. The function of the DV is to shunt the substrate-rich blood coming from the placenta via the umbilical vein to the heart. The DV diverts 25% of the blood, with the remainder being distributed to the liver and joining the circulation via the hepatic portal system.
The DV waveform can be detected by Doppler and is sensitive to cardiac function, which in turn is adversely affected by chronic severe decrease in substrate/oxygen availability. In response to hypoxia, the DV becomes more dilated and there is reduced flow during ventricular diastole, resulting in increased DV pulsatility index for veins (PIV), followed by increasingly retrograde flow during atrial systole, seen as absent or reversed a-wave ( Fig. 17.10 ).
The utility of the DV waveform is primarily in the very premature fetus with IUGR, or in the preterm fetus with abnormal UA waveforms. Reversal or absence of the DV a-wave (see Fig. 17.10 ), particularly in combination with umbilical vein pulsations, has been shown to be closely associated with an umbilical cord pH < 7.20 at delivery (65% sensitivity and 95% specificity). Similarly, these DV Doppler changes are associated with an 11-fold increase in major adverse neonatal outcomes and a doubling in neonatal mortality.
A recent study (TRUFFLE) used DV Doppler measures to assist in determining timing of delivery in preterm infants with IUGR. In cases where delivery was determined by increased DV pulsatility index or absent DV a-wave, perinatal mortality was 6% in control and 10% in the DV Doppler measures group. However, neurological impairment at 2 years of age was reduced in the measures group from 9% to 5%, respectively. In those for whom delivery timing was based on reduced and more complex measures of heart rate variability from the Doppler, perinatal mortality and abnormal 2-year outcomes were reduced at 7% compared to 15%, respectively. Although the outcomes were not significantly different between groups, the study suggests that delivery based on Doppler changes may provide better long-term outcomes, possibly at the expense of a small increase in perinatal mortality.
Sequence of Changes in Doppler Parameters in the Fetus With Intrauterine Growth Restriction
The traditional view of the changes in Doppler parameters was that as placental function deteriorated, there would be a clearly defined sequence of changes in Doppler findings with an initial increase in umbilical artery impedance (followed by changes in the waveform: absent end-diastolic flow [EDF] and then reversed EDF). As placental function deteriorated further, the reduction in oxygen and substrate to the fetus would result in a brain-sparing effect with a measurable reduction in the MCA impedance. Changes in the DV, initially with increased pulsatility index and then reversal of the a-wave, would be later signs, as the fetal myocardium became increasingly hypoxic and functioned suboptimally.
The recent PORTO study has challenged this viewpoint. This prospective study of 1116 fetuses with estimated fetal weight <10th centile demonstrated there is no single predominant pattern of Doppler changes. Nearly half (46%) of fetuses showed changes initially in the umbilical artery with pulsatility index >95th centile or absent or reversed EDF, 27% had MCA pulsatility index <5th centile, and 11% had abnormal DV measures (either pulsatility index >95th centile, or absent, or reversed a-wave.)
The pattern of adverse outcomes, such as intraventricular hemorrhage, periventricular leukomalacia, hypoxic ischemic encephalopathy, necrotizing enterocolitis, bronchopulmonary dysplasia, sepsis, and death, is also of interest. Eighty-six percent of fetuses with abnormal umbilical artery Doppler measures had adverse outcomes, compared to 51% with abnormal MCA and only 25% with abnormal DV Doppler measures. In contrast to the TRUFFLE study, this study included late preterm gestations, up to 36 weeks’ gestation. These findings demonstrate that the pattern of Doppler changes in a fetus with IUGR may vary significantly and that a combined set of measures from the umbilical cord, MCA, and the DV may provide complementary information from each of the measures that may assist the clinician in evaluating fetal risk.
Intrapartum Assessment
The occurrence of injury to brain during the birth process has been the focus of clinical research for more than a century. Considerable work has shown that brain injury in the intrapartum period does occur and affects a large absolute number of infants worldwide. It is obscure in most cases in terms of exact timing and precise mechanisms, awaits more sophisticated means of detection in utero, and represents potentially preventable neurological morbidity. Among the many adverse consequences of the increase in obstetrical litigation has been a tendency in some quarters of the medical profession to deny the importance, or even the existence, of intrapartum brain injury. This tendency is particularly unfortunate in that it is clear that true obstetrical malpractice is a rare occurrence and that the obstetrician is called on to deal with perhaps the most dangerous period in an individual’s life with inadequate methods. Recognition from experimental studies shows that a considerable proportion of hypoxic-ischemic brain injury evolves after cessation of the insult and can be interrupted to a considerable extent by several approaches (see Chapter 13 , Chapter 18 , Chapter 19 , Chapter 20 ). Therefore the ultimate possibility of intervention both in utero and in the early postnatal period is strongly suggested. Denial that intrapartum injury occurs may impair development and application of such brain-saving intervention.
Determination of the nature and timing of cerebral injury is challenging to determine. The most commonly cited marker of hypoxic-ischemic cerebral injury is the pattern of fetal heart rate. The alterations in fetal heart rate that occur with disturbances to fetal well-being have been defined in great detail in the past several decades with the widespread use of electronic fetal monitoring, usually supplemented with fetal blood sampling to assess acid-base status. The passage of meconium in utero is an often-cited but far less useful indicator of serious fetal distress (see later). In the following sections, we will review the basic elements of intrapartum assessment of the human fetus ( Table 17.7 ), namely, the implications of meconium passage in utero, the important fetal heart rate patterns, and the relation of fetal heart rate alterations to fetal acidosis and to neurological morbidity in the newborn period. Finally, we will briefly discuss certain other measures of fetal surveillance. In the first section that follows, the relationship between intrapartum asphyxia and cerebral palsy is reviewed.
|
Relationship Between Intrapartum Asphyxia and Cerebral Palsy
Numerous epidemiological studies have shown that most cases of cerebral palsy observed in children are not related to intrapartum asphyxia. Related clinical epidemiological data also support this conclusion.
The epidemiological data have been derived from studies of many thousands of infants born over the past 3 to 4 decades, including the era of modern perinatology and neonatology ( Table 17.8 ). Thus, if one excludes premature infants in whom the overwhelming balance of data shows that timing of injury is primarily postnatal (see Chapter 14 , Chapter 15 , Chapter 16 ), approximately 12% to 24% of cases of cerebral palsy can be related to intrapartum asphyxia. Indeed, if one considers the six large-scale studies of term infants born in the last 3 decades, the data are remarkably consistent in showing that 17% to 24% of cases of cerebral palsy are related to intrapartum asphyxia. A careful MRI study of 40 individuals with cerebral palsy also led to the conclusion that 17% to 24% of term infants sustained their injury from perinatal events.
| COUNTRY | YEARS OF INFANTS’ BIRTHS | PERCENTAGE RELATED TO ASPHYXIA |
|---|---|---|
| United States | 1959–1966 | 12% |
| Australia | 1975–1980 | 17% |
| Finland | 1978–1982 | 24% |
| Ireland | 1981–1983 | 23% |
| England | 1984–1987 | 17% |
| Sweden | 1987–1990 | 17% |
| Sweden | 1991–1994 | 24% |
Although the data just described indicate that the majority of children examined later with the diagnosis of cerebral palsy did not sustain intrapartum asphyxia, the findings have been interpreted by some clinicians to mean that intrapartum brain injury is rare or nonexistent and therefore unimportant. As noted in the introduction to this section, such a conclusion is incorrect. A sizable body of clinical and brain imaging data shows that brain injury occurs intrapartum in a large absolute number of infants (see Chapter 20 ). In view of the relatively high prevalence of cerebral palsy, in most countries, generally 2 to 3 cases per 1000 children born, even a relatively small percentage of cases caused by intrapartum events translates into a very large absolute number. (Consider the approximately 4 million live births and the 8000 to 9000 new cases of cerebral palsy in the United States yearly.) These points were stated eloquently in an exchange of communications in The Lancet ( Table 17.9 ).
| Editorial (Anonymous), November 25, 1989 |
| “In light of the evidence reviewed above, the continued willingness of doctors to reinforce the fable that intrapartum care is an important determinant of cerebral palsy can only be regarded as shooting the specialty of obstetrics in the foot.” |
| Letter to The Lancet a |
| “However medicolegally comforting the new epidemiological orthodoxy you espouse may be, most of us will continue to believe that severe hypoxia/ischemia is deleterious to the brain, that the longer it goes on the worse the effect, and that delayed, inefficient, or inappropriate treatment can be disastrous. It is no longer a matter for conjecture whether asphyxia and cerebral damage are causally related, or merely occur in the same antenatally imperfect individual. Ultrasonography, and many other objective tests of cerebral structure and function allow us to follow the time course of evolving neuronal damage in the postnatal period following severe asphyxia.” |
| “You suggest that by accepting ‘…the fable that intrapartum care is an important determinant of cerebral palsy,’ the specialty of obstetrics is shooting itself in the foot, and that it is time to look elsewhere. We are concerned that by ignoring the 23% of cerebral palsy that is related to intrapartum asphyxia, obstetricians and their colleagues will take the advice too literally and shoot themselves somewhere else.” |
a From Hope PL, Moorcraft J. Cerebral palsy in infants born during trial of intrapartum monitoring. Lancet . 1990;335:238, with permission.
The tasks for the future are to devise technologies that can aid in definition of the exact timing and mechanisms of this intrapartum brain injury and to develop interventions both during and after the insult that will prevent brain injury in the affected infants.
Meconium Passage in Utero
Fetal hypoxia may lead to meconium passage in utero secondary to increased intestinal peristalsis and, perhaps, also to relaxation of the anal sphincter. However, the increased vagal tone associated with fetal maturation may lead to meconium passage; approximately 10% to 20% of apparently normal pregnancies at term and 25% to 50% of postdate pregnancies are accompanied by meconium-stained amniotic fluid. Thus, although the presence of meconium-stained amniotic fluid during labor is a potentially ominous sign concerning fetal well-being, controversy exists over the relative importance of this sign. The discrepancy in conclusions may relate in part to the failure to assess the timing and quantity of meconium passed. In a prospective study of 2923 pregnancies, Meis and co-workers observed the presence of meconium-stained amniotic fluid in 646 (22%) of cases. Meconium passage was classified as either early (light or heavy) or late. Early passage referred to meconium noted on rupture of the fetal membranes before or during the active phase of labor; light or heavy designations were made on the basis of quantity (and color). Late passage referred to meconium-stained amniotic fluid passed in the second stage of labor, after clear fluid had been noted previously. Patients with early-light meconium-stained amniotic fluid constituted approximately 54% of the total group with stained fluid and were no more likely to be depressed at birth than were control patients. Patients with late passage of meconium constituted approximately 21% of the total group with stained fluid and exhibited 1- and 5-minute Apgar scores lower than 7 two to three times more often than did control patients, but this difference was not statistically significant. (In a subsequent study, the same investigators demonstrated that the presence of both late passage of meconium and certain intrapartum fetal heart rate abnormalities, i.e., loss of beat-to-beat variability and variable decelerations [see next section], sharply increased the likelihood of depressed Apgar scores. ) Finally, however, patients with early-heavy meconium-stained amniotic fluid, which constituted 25% of the total group, had a sharply increased likelihood of neonatal depression as well as intrapartum and neonatal death. Significantly, of this group 33% exhibited Apgar scores lower than 7 at 1 minute, and 6.3% had scores lower than 7 at 5 minutes. Early-heavy meconium-stained amniotic fluid was also associated with other signs of fetal distress (e.g., fetal heart rate abnormalities ) and with antecedent obstetrical conditions that lead to neonatal morbidity. Thus, the data suggest that the timing and quantity of meconium passage are critical variables in attempting to assess the significance of this occurrence for fetal well-being. Presumably, these two aspects of meconium passage correlate with the duration and severity of the intrauterine insult. Clinical estimation of the timing of meconium passage in utero is aided by examination of placental membranes or of the newborn ( Table 17.10 ). In general, in most cases , the finding of meconium-stained amniotic fluid is not of serious import concerning intrauterine asphyxia. Moreover, in view of the high rate of meconium passage without serious perinatal complications, the most prevalent current view is that “the presence of meconium per se does not imply fetal distress during labor until other parameters, e.g., fetal heart rate abnormalities, support such a contention.” However, a recent study continues to confirm the association of thick meconium with acute hypoxic-ischemic cerebral injury. In this study of 405 infants >35 weeks gestation with early encephalopathy, clinical markers, and neuroimaging consistent with hypoxic-ischemic injury, 29% had thick meconium at delivery versus 7% of controls. On multivariable analysis, thick meconium was one of seven intrapartum factors that was independently associated with hypoxic-ischemic injury.
| CLINICOPATHOLOGICAL FEATURE | PROBABLE DURATION BEFORE BIRTH |
|---|---|
| Pigment-laden macrophages in amnion | >1 hour |
| Pigment-laden macrophages in chorion | >3 hour |
| Meconium-stained fetal nails | >4–6 hour |
Fetal Heart Rate Alterations
In most medical centers, the central means of the intrapartum assessment of fetal well-being is electronic fetal monitoring. Evaluation of fetal heart rate, particularly in relation to uterine contractions, is the most widely used form of electronic fetal monitoring. Although the necessity and relative merits of electronic fetal heart rate monitoring have been the subjects of disagreement, a
a References .
utilization of such monitoring during labor has been standard obstetrical practice in the United States. The bases for the major controversy concerning the value of electronic monitoring of the fetal heart rate are that (1) the abnormalities are detected in labor in a large number of infants who are normal at birth and on follow-up, and (2) the increase in operative deliveries provoked by the finding of such abnormalities has had little or no impact on adverse neurological outcome, particularly cerebral palsy. It is beyond the scope of this book to discuss in detail the relative merits of the use of electronic fetal monitoring in all pregnancies versus use in high-risk pregnancies only. It is perhaps worthy of emphasis only that in the so-called Dublin trial of nearly 13,000 women, a study generally acknowledged to be among the best designed of all trials, the use of electronic fetal monitoring was followed by a decrease in the incidence of neonatal seizures, and the presence of certain heart rate patterns (see subsequent discussion) was an important predictor of abnormal neonatal neurological examinations. A decrease in neonatal seizures was documented in a meta-analysis of 12 studies involving 59,324 infants. In another well-designed study, 27% of the 78 patients with cerebral palsy who had intrapartum fetal monitoring exhibited multiple late decelerations or decreased beat-to-beat variability of the heart rate. In a further study of 405 infants with proven neonatal hypoxic-ischemic injury, abnormal fetal heart rate tracing was observed in 77% and was independently associated with disease with an odds ratio of 12.75.The major aspects of the fetal heart rate pattern evaluated are divided into baseline features (i.e., rate and beat-to-beat variability) and periodic features (i.e., accelerations or decelerations), usually in relation to uterine contractions ( Fig. 17.11 and Table 17.11 ). The significance of these aspects of the fetal heart rate is discussed in detail in standard writings on maternal-fetal medicine. A brief overview is provided next.
| FETAL HEART RATE PATTERN | MAJOR CAUSE | USUAL SIGNIFICANCE |
|---|---|---|
| Loss of beat-to-beat variability | Multiple | Variable |
| Early decelerations | Head compression | Benign |
| Late decelerations | Uteroplacental insufficiency | Ominous |
| Variable decelerations | Umbilical cord compression | Variable |
Rate
Assessment of the fetal heart rate begins with the finding that the normal heart rate (± 2 standard deviations) is 120 to 160 beats/minute (see Fig. 17.11 ). Abnormalities of baseline fetal heart rate are suspicious, but in the absence of disturbances of beat-to-beat variability or decelerations (see later discussions), these abnormalities usually do not reflect an ominous event, such as severe fetal hypoxia. The most common cause of baseline tachycardia in the fetus is maternal fever secondary to amnionitis. Maternal fever can also occur following maternal epidural administration, particularly as many as >75% of women in labor in developed countries will receive epidural for pain relief. Other causes include fetal infection, certain drugs (e.g., atropine and beta-sympathomimetics), arrhythmia, and maternal anxiety. Fixed tachycardia with loss of beat-to-beat variability, especially in relation to patterns of deceleration, may be observed with fetal hypoxia and has been observed in infants before intrapartum or early neonatal death. In these instances, the tachycardia may reflect a fetal response to massive blood loss, since this is the best compensatory mechanism to maintain cardiac output given the limitations on stroke volume ( Fig. 17.12 ).
Baseline bradycardia with average beat-to-beat variability and no sign of fetal compromise is observed most commonly in the postmature fetus. Bradycardia may be observed with fetal heart block, as a drug effect and with hypothermia. Baseline bradycardia as a feature of fetal hypoxia is accompanied by loss of beat-to-beat variability and decelerations.
Beat-to-Beat Variability
Normal fetal heart rate exhibits fluctuations of approximately 6 to 25 beats/minute (see Fig. 17.11 ). This beat-to-beat variability reflects the modulation of heart rate by autonomic, particularly parasympathetic, input and especially depends on inputs from cerebral cortex, diencephalon, and upper brain stem to the cardiac centers in the medulla and then to the vagus nerve. Of the autonomic input, parasympathetic influences are more important than sympathetic influences. The presence of normal beat-to-beat variability is considered the best single assessment of fetal well-being . Indeed, the presence of normal variability is a reassuring finding in the presence of the mild variable decelerations common in the second stage of labor. Loss of or diminished beat-to-beat variability may be observed not only with significant fetal hypoxia but also with prematurity, fetal sleep, drugs (e.g., sedative-hypnotics, narcotic-analgesics, benzodiazepines, atropine, and local anesthetics), congenital malformations (e.g., anencephaly), and intrauterine, a ntepartum cerebral destruction. a
a References .
The loss of beat-to-beat variability coupled with variable or late decelerations (see subsequent sections) significantly enhances the likelihood that the fetus is undergoing significant hypoxia . The importance of careful longitudinal assessment of heart rate variability has been suggested. Ample documentation has shown the association between decreased fetal heart rate variability and decelerations, fetal acidosis, intrauterine fetal death, and low Apgar scores.Accelerations
Increases or decreases in fetal heart rate associated particularly with contractions are designated accelerations or decelerations and constitute the periodic features of the fetal heart rate. Accelerations during the uterine contractions of labor, as in the case of antepartum contractions (see previous discussion) or with fetal movement, are not of concern and in fact are generally considered a sign of fetal well-being. Uncommonly, heart rate accelerations may be an early sign of compression of the umbilical vein. Maintenance of fetal heart rate variability is a reassuring sign of fetal well-being in the presence of such accelerations.
Decelerations
Decelerations are of three major types: early, late, and variable ( Figs. 17.13–17.15 ; see Table 17.11 ). These decreases in heart rate associated with uterine contraction have significantly different mechanisms and implications for outcome.
Early Type.
An early deceleration is one that begins with the onset of a contraction, reaches its peak with the peak of the contraction, and then returns to normal baseline levels as the contraction ends (see Fig. 17.13 ). These decelerations appear to be related to compression of the fetal head and are mediated by vagal input to the heart. The mechanism of this effect of head compression may relate to a transient increase in intracranial pressure with secondary hypertension and bradycardia through the Cushing reflex. Early decelerations are not associated with fetal hypoxia, as reflected in fetal acid-base measurements or in neonatal depression.
Late Type.
A late deceleration is one that begins after a contraction starts, but reaches a peak well after the peak of contraction is reached and does not return to baseline until 30 to 60 seconds after the contraction is completed (see Fig. 17.14 ). These decelerations are related primarily to uteroplacental insufficiency (e.g., placental disorder, uterine hyperactivity, and maternal hypotension) and are mediated by fetal hypoxia (see Table 17.11 ). a
a References .
Such decelerations are unusual with fetal scalp pressure of oxygen (PO 2 ) greater than 20 mm Hg, but appear in more than 50% of infants with fetal scalp PO 2 less than 10 mm Hg. It is understandable that fetal hypoxia occurs after the onset of a uterine contraction when uteroplacental insufficiency is present, because uterine contractions normally reduce uterine blood flow and thereby oxygen delivery to the fetus. Fetal hypoxia causes bradycardia by a multifactorial mechanism that primarily includes a chemoreceptor-mediated vagal response initially and then a direct effect on myocardial function. The initial reflex vagally mediated response is accompanied by normal fetal heart rate variability and thus “normal CNS integrity,” whereas the nonreflex myocardial late deceleration is observed without heart rate variability and thus “inadequate fetal cerebral and myocardial oxygenation.”The causal relationship between fetal hypoxia and late decelerations has been shown in several ways. First, as just noted, the decelerations have been correlated temporally with fetal hypoxia, identified with fetal capillary blood sampling and tissue oxygen electrodes. Second, when fetal oxygenation is improved by the administration of 100% oxygen to the normotensive mother or of intravenous fluids and pressors to the hypotensive mother, the bradycardia may cease. Third, a strong correlation exists between the occurrence of late decelerations and alterations in fetal acid-base status secondary to fetal hypoxia.
The possibility that the late decelerations may have secondary deleterious effects was suggested by studies in subhuman primates that showed that late decelerations are accompanied not only by fetal hypoxia and acidosis but also by hypotension. The bradycardia per se appeared to cause the hypotension. Moreover, studies with fetal sheep documented decreased cardiac output with bradycardia, particularly at rates lower than 60 beats/min. Data on cerebral blood flow are lacking, however.
The duration of asphyxia with late decelerations required to produce brain injury is not entirely clear, although experiments with fetal monkeys suggested that time periods less than 1 hour are not generally sufficient. Studies of human infants also suggested that a time period of less than 1 hour is not likely to be harmful. However, this conclusion must be made very cautiously because the severity of the insult is critical and has not been studied systematically with regard to the timing required to produce fetal brain injury. Indeed, in the case of severe, abrupt, terminal insults (i.e., acute total asphyxia just before delivery), brain injury appears to occur after insults of less than 1 hour.
Variable Type.
The most commonly observed fetal heart rate deceleration is variable deceleration , which occurs in a substantial minority of all fetuses (see Fig. 17.15 ). This characteristically abrupt slowing of the fetal heart rate may begin before, with, or after the onset of the uterine contraction and is variable in duration. The deceleration pattern is principally the result of varying degrees of umbilical cord compression (see Table 17.11 ). Thus, this periodic pattern is more common with nuchal, short, or prolapsed umbilical cord or decreased amniotic fluid volume (oligohydramnios, ruptured membranes). The mechanism of the bradycardia is considered to be an increase in peripheral resistance, which leads to fetal hypertension that, in turn, causes baroreceptor-stimulated, vagally mediated bradycardia. Occasionally, the umbilical cord compression with each contraction can be prevented by alteration of maternal position. Distinction of early from late cord compression can be made on the basis of determinations of fetal carbon dioxide pressure (PCO 2 ) and base excess; thus, respiratory acidosis reflects early umbilical cord compression with impaired umbilical blood flow, and metabolic acidosis indicates late cord compression with fetal tissue hypoxia. When variable decelerations are accompanied by or evolve into late decelerations, or when beat-to-beat variability is diminished or lost (even without late decelerations), the likelihood of significant fetal hypoxia is markedly enhanced.
Taxonomy of Fetal Heart Rate Patterns
The currently accepted taxonomy, endorsed by the American College of Obstetricians and Gynecologists (ACOG), divides all patterns of EFM into 3 categories: category I (normal), category II (indeterminate), and category III (abnormal) (see Fig. 17.12 , Table 17.12 ), based on the ability to predict acid-base status at the time. The ACOG recommendations concerning the timing of monitoring do not provide instructions regarding longitudinal fetal heart rate assessments. Some investigators consider careful longitudinal assessment during labor, especially considering the evolution of category II patterns, critical for early detection of the deteriorating fetus.
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