Chapter 7. Hypoxic-Ischemic Encephalopathy: Intrauterine Assessment

326

TABLE 7-1



UNIT III



HYPOXIC-ISCHEMIC ENCEPHALOPATHY



48



Major Means of Antepartum

Assessment of the Human Fetus



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 movements/hr



40



Fetal Movement

Detection by maternal perception or by real-time

ultrasonography



32

24

16

8



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



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 Figure 7-2. Decreased fetal movements perceived by the mother over the 7 days before delivery

could 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).12

The most common denominator of fetal inactivity

was chronic uteroplacental insufficiency. In another study

in which pregnant women 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.17 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.

Subsequent work also indicates the value of assessment

of fetal movements in the evaluation of fetal condition.18,21,38-40 Overall, the data show the value of this

approach in identifying the infant who may be exhibiting signs of cerebral dysfunction and who may be

vulnerable to injury imminently or by the processes

of later labor and vaginal delivery, or both.

Fetal Neurological Examination

The observations described in the preceding paragraphs are reminiscent of many of those made during

TABLE 7-2



26



28



30



36

34

32

38

Gestation (wk)



40



42



44



Figure 7-1 Relation of quantity of fetal movement to gestational

age. Movements were quantitated by maternal perception. (From

Rayburn WF: Antepartum fetal assessment: Monitoring fetal activity,

Clin Perinatol 9:231-240, 1982.)



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 large 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 3) is obvious, and, indeed, 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.21,22,41-47 Finally, detailed analysis

of the quantity and quality of fetal breathing can provide

still further information about the fetal nervous

system.15,21,34,36,48,49 With the wide use of real-time

ultrasonography, the standardization of the neurological phenomena observable, and, most important and

still most difficult, the correlation of aberrations with

the topography of neuropathology, highly valuable

evaluation of the fetal central nervous system and

dysfunction thereof 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



Fetal Behavioral States at 38 Weeks of Gestation*



State{



Body Movements



Eye Movements



Fetal Heart Rate Pattern



1F

2F

3F

4F



Absent (occasional startle)

Present (frequent bursts)

Absent

Present (almost continuous)



Absent

Present

Present

Present (continuous)



Narrow variability, isolated acceleration

Wide variability, acceleration with movement

Wide variability, no accelerations

Long accelerations or sustained tachycardia



*See text for references.

{

These fetal states approximate neonatal behavioral states, that is, quiet sleep (1F), active sleep (2F), quiet waking (3F), and active waking (4F).



Chapter 7

40

36

Fetal movements/hr



32

Favorable

perinatal

outcome

(N = 1037, 89%)



28

24

20

16



Unfavorable

perinatal

outcome

(N = 124, 11%)



12

8

4

7



6



5



1

3

2

4

Days prior to delivery



Figure 7-2 Relation of decrease in quantity of fetal movement over

7 days before delivery to unfavorable perinatal outcome. See text for

details. (From Rayburn WF: Antepartum fetal assessment: Monitoring

fetal activity, Clin Perinatol 9:231-240, 1982.)



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 7-1).

Nonstress Test

Of the two techniques, the so-called nonstress test is the

approach used as an initial evaluation.50-53 In general,

the particular value of the technique is the determination of a healthy fetus,50,51,53-55 based on the 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/minute and last at least 15 seconds, and

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.21,47,51-53

Concerning 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.47,50,51

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, both 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 maternalfetal 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.53



Hypoxic-Ischemic Encephalopathy: Intrauterine Assessment



327



Contraction Stress Test

The so-called contraction stress test in the past was most

commonly used 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.53-56 The

established clinical as well as 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, which can be

stimulated by breast stimulation or oxytocin infusion.53,57-60 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. Concerning the predictive value of

a positive stress test, 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,

and the higher value was for those with nonreactive

positive tests).58-60 Thus, the stress test is of value

in predicting the infant at risk for intrapartum

disturbances.

Currently, the contraction stress test is no longer

the principal method for follow-up in most centers.53

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.53

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.52,53,61-69 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 7-1). 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



328



UNIT III



HYPOXIC-ISCHEMIC ENCEPHALOPATHY



7.40



250



225



200



7.30



Cerebral palsy rate per 1000 live births



Antepartum umbilical venous pH



7.35



7.25



7.20



7.10



175



150



125



100



75



50



7.05

10



6

2

8

4

Fetal biophysical profile score



0



Figure 7-3 Relation of fetal biophysical profile (BPP) score to mean

umbilical vein pH (±2 SD) in fetal blood obtained by cordocentesis.

A progressive and highly significant direct linear relationship exists

between abnormal BPP scores ( 6) and umbilical vein pH (P <.01).

Asterisks denote a significantly lower mean pH compared with the

value recorded for the immediately higher BPP score. (From Manning

FA: Fetal assessment by evaluation of biophysical variables. In Creasy

RK, Resnik R, editors: Maternal-Fetal Medicine, 4th ed, Philadelphia:

1999, WB Saunders.)



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 Figure 7-3, which illustrate the relation of

the fetal biophysical score to umbilical venous pH determined by cordocentesis.40 Similar correlations are available regarding incidence of meconium passage during

labor, signs of intrapartum fetal distress, and perinatal

mortality.53,64 Of particular importance, the degree of

abnormality of the fetal biophysical score has been

shown to correlate with the occurrence of brain injury

that results in cerebral palsy (Fig. 7-4).53,69 Data from a

single center suggested that alterations in obstetrical

management provoked by the results of the score

could lead to a three- to fourfold decline in cerebral

palsy rates.69 Although the procedure requires expertise

in ultrasonography and experience in recognition of the

phenomena, the value of the profile is striking. The role

of this technique in the detection of acute and chronic

intrauterine asphyxia and in the prevention of further

injury by appropriate management of the remainder of

the pregnancy and the delivery can be substantial

(Table 7-3).

Fetal Growth

As with other antepartum assessments, advances in

ultrasound technology have provided the capability of

accurate quantitative assessment of fetal growth.7,70

The particular value of this assessment is in the



25



0

Normal

6

(N = 21856) (N = 324)



4

(N = 117)



2

(N = 35)



0

(N = 4)



Biophysical profile score



Figure 7-4 Relationship between last fetal biophysical profile score

and incidence of cerebral palsy. An inverse, exponential, and highly

significant relationship is apparent (P <.001). (From Harman CR:

Assessment of fetal health. In Creasy RK, Resnik R, Iams JD, editors:

Maternal-Fetal Medicine: Principles and Practice, 5th ed, Philadelphia:

2004, WB Saunders.)



detection of intrauterine growth retardation (see

Table 7-1), although other aberrations of growth

(e.g., large body size and large head) have important

implications for management of labor and 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.7 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). Moreover, 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.7,71-77 In one

series from a single high-risk service, 35% of growthretarded fetuses exhibited intrapartum fetal heart rate

abnormalities indicative of fetal distress.72 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.73

Moreover, growth-retarded infants with intrapartum

fetal heart decelerations demonstrate considerably



Chapter 7

TABLE 7-3



4/10

10/10



329



Fetal Biophysical Score: Relation to Outcome and Recommended Management



Biophysical

Profile Score*

0/10

2/10



Hypoxic-Ischemic Encephalopathy: Intrauterine Assessment



Interpretation

Severe acute asphyxia

Acute fetal asphyxia, most likely

with chronic decompensation

Acute fetal asphyxia likely; if oligohydramnios present, chronic

asphyxia also very likely

No evidence of fetal asphyxia



Predicted Perinatal

Mortality

60/100

125/100

9.1/100

<0.1/100



Recommended Management

Immediate delivery by cesarean section

Delivery for fetal indications (usually

cesarean section)

Delivery by obstetrically appropriate method

with continuous monitoring

No acute intervention



*Values intermediate between 4/10 and 10/10 not shown; see Harman CR: Assessment of fetal health. In Creasy RK, Resnik R, Iams JD, editors:

Maternal-Fetal Medicine: Principles and Practice, 5th ed, Philadelphia: WB Saunders, 2004.

Adapted from Harman CR: Assessment of fetal health. In Creasy RK, Resnik R, Iams JD, editors: Maternal-Fetal Medicine: Principles and Practice,

5th ed, Philadelphia: WB Saunders, 2004.



higher umbilical artery lactate levels than do normally

grown infants with similar decelerations.74 Thus,

growth-retarded infants tolerate labor less well than

do normally grown infants, perhaps in part because

of deficient stores of glycogen in liver, heart, and, possibly, 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 Umbilical and Fetal Cerebral

Vessels

The application of the Doppler technique to the study

of blood flow velocity in umbilical vessels has led to an

enormous literature. The potential value of determination of blood flow and vascular resistance in elucidation

of a wide variety of disease processes in both the pregnant woman and her fetus clearly is great. The basic

principles of the Doppler technique are reviewed in

Chapter 4 in relation to neonatal studies of the cerebral

circulation and are not reiterated here. In the following

section, I review separately studies of umbilical and

fetal cerebral vessels, particularly the umbilical artery

and the fetal middle cerebral artery.

Umbilical Artery

Most studies based on the use of Doppler in pregnancy

have focused on the umbilical artery.18,53,71,75,76,78-93

The principal quantitative parameters of the Doppler

waveform used have been the pulsatility index of Gosling

(peak systolic velocity [S] À end diastolic velocity [D]/

mean velocity), the resistance index of Pourcelot (S À D/S),

and the S/D ratio. The values of these ratios, in general,

are not affected by the angle of insonation, clearly

difficult to maintain constant in the clinical situation.

The pulsatility index and the resistance index reflect, in

largest part, vascular resistance. The principal change

in umbilical artery blood flow velocity with progression

of normal pregnancy is a decline in the resistance parameters.53,79,81,87,94 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.95 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. 7-5).96

The major application of Doppler studies of blood

flow velocity in the umbilical artery has been in the

investigation of the fetus with intrauterine growth

retardation and the complications associated with

this fetal state.* In intrauterine growth retardation,

the principal finding is an increase in the resistance

measures.{ 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. 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.103 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. 7-6).104 The clinical predictive value of the

diastolic flow in the umbilical artery was apparent in

a study of 459 high-risk pregnancies.94 Thus, the rate

of fetal or neonatal death in the presence of end

diastolic flow was 4% and increased to 41% with

absence of flow and to 75% with reversal of flow.

With prompt and detailed further fetal assessments

and appropriate interventions, the unfavorable outlook

with absence of diastolic flow has not been so

marked.53,107 However, reversal of flow is associated

with a considerable risk of fetal compromise, perinatal

mortality, neonatal neurological disturbances, and



*See references 18,53,71,75,76,78-80,82,83,85-87,89-94,97-107a.

{

See references 18,71,75,76,79,80,86,87,89-94,97,99,106.



HYPOXIC-ISCHEMIC ENCEPHALOPATHY



10



8

6

n = 74

r = 0.82

y = 0.027 + 0.021x



4



18



A



24

30

36

Gestational age (wk)



Umbilical venous flow (mL/min)



UNIT III

Umbilical vein diameter (cm)



330



540

420



n = 74

r = 0.86

log y = 1.09 + 0.04x



300

180

60



42



18



B



36

24

30

Gestational age (wk)



42



Figure 7-5 Relationship between umbilical vein diameter and umbilical venous flow in human pregnancy. A, umbilical vein diameter. B,

Umbilical venous flow. Note the linear increase in venous diameter and the exponential increase in blood flow. (From Sutton MS, Theard MA,

Bhatia SJ, et al: Changes in placental blood flow in the normal human fetus with gestational age, Pediatr Res 28:383-387, 1990.)



subsequent neurodevelopmental disability, with the

magnitude of risk varying considerably with the

selection of the population studied.

The central abnormality in the growth-retarded fetus

leading to the increase in placental vascular resistance is

a disturbance in placental vessels.108 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.109 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.53 Thus, the value of this

4



technique in the evaluation of a wide variety of high-risk

pregnancies is very high.

Fetal Cerebral Vessels

Following soon after the initial applications of Doppler

for study of umbilical blood flow velocity was the successful study of blood flow velocity in fetal cerebral

vessels, particularly the middle cerebral artery. 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. 7-7).53,87,94,110-115

Additionally, mean cerebral blood flow velocity has

been shown to increase during the same period that

resistance appears to decrease.111 This combination

of findings suggests an increase in cerebral blood flow

100

95

90



2



Resistance index



Lactate (mmol/L)



3



0

0



0.5



1.0

2.5

1.5

2.0

Pulsatility index: umbilical artery



3.0



Figure 7-6 Relationship between lactate concentration of fetal

blood (sampled from the umbilical vein [solid circles] or artery

[open circles] at the time of cesarean section) and pulsatility index

obtained from the umbilical artery before delivery. Note the marked

increase in fetal blood lactate with increasing pulsatility index (i.e.,

increasing placental vascular resistance). (From Ferrazzi E, Pardi G,

Bauscaglia M, et al: The correlation of biochemical monitoring versus

umbilical flow velocity measurements of the human fetus, Am J Obstet

Gynecol 159:1081-1087, 1988.)



90th



60

55



1



85

80

75

70

65



10th



50



25-28



29-32



37-40

33-36

Gestational week



41-42



Figure 7-7 Resistance index values of fetal intracranial arterial

velocity waveforms in normal pregnancies. The framed areas represent the values between the 25th and 75th percentiles for each gestational age period. The medians (horizontal lines within the framed

areas) and the 10th and 90th percentiles are indicated. Note the sharp

decline in the last month of pregnancy. (From Kirkinen P, Muller R,

¨

Huch R, Huch A: Blood flow velocity waveforms in human fetal intracranial arteries, Obstet Gynecol 70:617-621, 1987.)



Chapter 7



Resistance index



100

95

90

85

80

75

70

65

60

55

50

45

40

26



Hypoxic-Ischemic Encephalopathy: Intrauterine Assessment

TABLE 7-4



Neonatal Outcome as a Function of

Ratio of Cerebral-Umbilical Pulsatility

Index

Ratio*<1.08

(n = 18)



90th



10th



28



30



34

36

32

Gestational week



38



40



42



Figure 7-8 Resistance index values in fetal intracranial arteries of

small-for-dates newborns (asterisks). The 10th and 90th percentiles

for normal pregnancy are indicated by the lines. Note the lower resistance values in the small-for-dates newborns. (From Kirkinen P, Muller

¨

R, Huch R, Huch A: Blood flow velocity waveforms in human fetal intracranial arteries, Obstet Gynecol 70:617-621, 1987.)



during the last trimester of pregnancy, perhaps related

to cerebral vasodilation or development of vascular

beds, or both. A particular role for the 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).111,116

As with Doppler studies of the umbilical vessels,

study of cerebral blood flow velocity has been directed

most commonly 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. 7-8).53,71,90,92-94,107a,

110,114,117-123 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 7-4).124

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.110,125 This observation

is identical to that made postnatally with posthemorrhagic hydrocephalus (see Chapters 4 and 11), 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



331



Small for gestational age

Cesarean section

(for fetal distress)

Umbilical vein pH (mean)

Five-minute Apgar score <7

Neonatal complications{



Ratio* >1.08

(n = 72)



100%



38%



89%

7.25

17%

33%



12%

7.33

3%

1%



*Ratio of pulsatility index from cerebral circulation to index from umbilical artery; normal mean value is approximately 2.0.

{

Intracerebral hemorrhage, seizures, respiratory distress syndrome.

Data from Gramellini D, Folli MC, Raboni S, et al: Cerebral-umbilical

Doppler ratio as a predictor of adverse perinatal outcome, Obstet

Gynecol 79:416-420, 1992.



have also been documented with changes in fetal

behavioral states and after administration of indomethacin to the mother.119,126

INTRAPARTUM ASSESSMENT

The occurrence of injury to brain during the birth

process has been the focus of clinical research for

more than a century. In my view, work has shown that

brain injury in the intrapartum period does occur,

affects a large absolute number of infants worldwide, is

obscure in most cases in terms of exact timing and precise mechanisms, awaits more sophisticated means of

detection in utero, and represents a large source of

potentially preventable neurological morbidity. Among

the many adverse consequences of the explosion 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. Although

it is unequivocally 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, this tendency is particularly unfortunate. With the recognition from

experimental studies that much of hypoxic-ischemic

brain injury evolves after cessation of the insult and

can be interrupted to a considerable extent by several

approaches (see Chapters 6 and 8), 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.

In general, the hallmark of intrapartum asphyxia has

been the occurrence of specific fetal heart rate abnormalities. The passage of meconium in utero is an oftencited but far less useful indicator of serious fetal

distress. 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, sometimes

supplemented with fetal blood sampling to assess

acid-base status. In the following sections, I review

the basic elements of intrapartum assessment of the



332

TABLE 7-5



UNIT III



HYPOXIC-ISCHEMIC ENCEPHALOPATHY



Major Means of Intrapartum

Assessment of the Fetus



Meconium passage

Fetal heart rate

Fetal acid-base status

Other techniques

Transcutaneous monitoring of blood gases and pH

Near-infrared spectroscopy

Doppler measurements of fetal blood flow velocity

Fetal electroencephalogram



human fetus (Table 7-5), 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, I 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.127-136 Related clinical epidemiological data also support this conclusion.69,136-148 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 7-6).

Thus, if one excludes premature infants, in whom the

overwhelming balance of data shows that timing of

injury is primarily postnatal (see Chapters 8 and 9),

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.149,150

Although the data just described indicate that the

majority of children examined later with the diagnosis

TABLE 7-6



Relationship between Intrapartum

Asphyxia and Cerebral Palsy: Term

Infants*



Country



Years of

Infants’ Births



United States

Australia

Finland

Ireland

England

Sweden

Sweden



1959-1966

1975-1980

1978-1982

1981-1983

1984-1987

1987-1990

1991-1994



*See text for references.



Percentage

Related to ‘‘Asphyxia’’

12%

17%

24%

23%

17%

17%

24%



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 large body of clinical and brain imaging data shows

that brain injury occurs intrapartum in a large absolute

number of infants. Indeed, 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 7-7).151 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 relaxation of the anal sphincter. However,

the increased vagal tone associated with fetal maturation may lead to meconium passage; approximately



TABLE 7-7



Interesting Exchanges Published in

The Lancet Concerning Intrapartum

Events and Cerebral Palsy



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*

‘‘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 ‘ðthe 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.’’

*From Hope PL, Moorcraft J: Cerebral palsy in infants born during trial

of intrapartum monitoring, Lancet 335:238, 1990.



Chapter 7



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.152-169 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-workers161

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.163) Finally, however, patients with ‘‘earlyheavy’’ 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. Indeed, 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 the newborn (Table 7-8).170

In general, in most cases, the finding of meconiumstained 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.’’169



Hypoxic-Ischemic Encephalopathy: Intrauterine Assessment

TABLE 7-8



333



Timing of Meconium Passage before

Birth



Clinical-Pathological Feature



Probable Duration

before Birth



Pigment-laden macrophages in amnion >1 hr

Pigment-laden macrophages in chorion >3 hr

Meconium-stained fetal nails

>4-6 hr

Data from Miller PW, Coen RW, Benirschke K: Dating the time interval

from meconium passage to birth, Obstet Gynecol 66:459-462,

1985.



Fetal Heart Rate Alterations

In most medical centers, the central means of the intrapartum assessment of fetal well-being is electronic

fetal monitoring.164,168,171-188 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,164,168,171,174,175,181,184-201a

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.135,196

A decrease in neonatal seizures was documented in a

meta-analysis of 12 studies involving 59,324 infants.185

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.186

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. 7-9 and Table 7-9). The

significance of these aspects of the fetal heart rate is

discussed in detail in standard writings on maternalfetal medicine. A brief overview is provided next.

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. 7-9).164,202



334



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Figure 7-9 Fetal heart rate tracing, normal pattern. The upper trace represents the fetal heart rate, and the lower trace represents uterine

activity. The fetal heart rate ranges generally between 130 and 150 beats/minute, with normal beat-to-beat variability of approximately 10 to 15

beats/minute. The uterine contractions shown are approximately 5 minutes apart. (Courtesy of Dr. Barry Schifrin.)



Abnormalities of baseline fetal heart rate are suspicious, but in the absence of disturbances of beat-tobeat variability or decelerations (see later discussions),

these abnormalities usually do not reflect an ominous

event, such as severe fetal hypoxia.164,188 The most

common cause of baseline tachycardia in the fetus is

maternal fever secondary to amnionitis. 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 may be observed with fetal hypoxia and has

been observed in infants before intrapartum or early

neonatal death.203

Baseline bradycardia with average beat-to-beat

variability and no sign of fetal compromise is

observed most commonly in the postmature fetus.164

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. 7-9).188,204,205



TABLE 7-9



Fetal Heart Rate Patterns: Major

Causes and Usual Significance



Fetal Heart Rate

Pattern



Major

Cause



Usual

Significance



Loss of beat-to-beat

variability

Early decelerations

Late decelerations



Multiple



Variable



Head compression

Uteroplacental

insufficiency

Umbilical cord

compression



Benign

Ominous



Variable decelerations



Variable



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.164,172,188,206-208 Of the autonomic input, parasympathetic influences are more important than sympathetic influences.188,209-211 The presence of normal beatto-beat variability is considered the best single assessment of

fetal well-being. 164,188,202,208 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.164 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, narcoticanalgesics, benzodiazepines, atropine, and local anesthetics), congenital malformations (e.g., anencephaly),

and intrauterine, antepartum cerebral destruction.164,172,188,202,208,212-214 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.164,172,188,202,208

Indeed, ample documentation has shown the association between decreased fetal heart rate variability and

decelerations, fetal acidosis, intrauterine fetal death,

and low Apgar scores.164,188,208,209

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.164,215,216

Uncommonly, heart rate accelerations may be an

early sign of compression of the umbilical vein.164,217



Chapter 7

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335



Hypoxic-Ischemic Encephalopathy: Intrauterine Assessment



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Figure 7-10 Fetal heart rate tracing, early deceleration. Note the typical early deceleration (i.e., the deceleration begins with the onset of the

contraction, reaches its peak with the peak of the contraction, and returns to a normal baseline as the contraction ends). Variability is

preserved. (Courtesy of Dr. Barry Schifrin.)



Maintenance of fetal heart rate variability is a reassuring

sign of fetal well-being in the presence of such

accelerations.



until 30 to 60 seconds after the contraction is completed

(see Fig. 7-11).164,188,201a,224 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 7-9).164,180,188,201a,208,225-230 Such decelerations

are unusual with fetal scalp pressure of oxygen (PO2)

greater than 20 mm Hg but appear in more than 50%

of infants with fetal scalp PO2 less than 10 mm Hg.231 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.180,232 Fetal hypoxia

causes bradycardia by a multifactorial mechanism that

primarily includes initially a chemoreceptor-mediated

vagal response and then a direct effect on myocardial

function.180,229,230,233 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.’’188

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.225,231



Decelerations

Decelerations are of three major types: early, late, and

variable (Figs. 7-10 to 7-12; see Table 7-9). 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.

7-10).164,188,218,219 These decelerations appear to be

related to compression of the fetal head and are

mediated by vagal input to the heart.220-222 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.164,196,223

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

17



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Figure 7-11 Fetal heart rate tracing, late deceleration. Note the late decelerations (i.e., the peak of the deceleration is reached well after the

peak of the contraction). The absent variability is consistent with decreased cerebral oxygenation. (Courtesy of Dr. Barry Schifrin.)



336



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Figure 7-12 Fetal heart rate tracing, variable deceleration. Note the recurrent variable decelerations, as described in the text, associated here

with maternal pushing, evidenced by the spikes in uterine activity (lower trace). The decreasing variability is concerning for recurrent ischemia and

fetal compromise. (Courtesy of Dr. Barry Schifrin.)



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 acidbase status secondary to fetal hypoxia.227

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.226 Moreover, studies with

fetal sheep documented decreased cardiac output with

bradycardia, particularly at rates lower than 60 beats/

minute.47,230,234,235 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.236 Studies of human infants also suggested

that a time period of less than 1 hour is not likely to be

harmful.237,238 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. 239,240

Variable Type. The most commonly observed fetal

heart rate deceleration is variable deceleration,164,202

which occurs in a substantial minority of all fetuses

(see Fig. 7-12).181,241 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 7-9).47,164,172,219,227 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.242 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 (PCO2) 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.243

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.164,188,200,227,241

Relation of Fetal Heart Rate Abnormalities to

Neonatal Neurological Course and Subsequent

Outcome

A distinct relationship has been demonstrated between

intrapartum abnormalities of fetal heart rate, sometimes with documented fetal acidosis, and neurological

morbidity in the neonatal period and after 1 year of

follow-up.188,196,201a,237,238,244-248 In a prospective

study, 50 infants of high-risk mothers who were provided intrauterine fetal heart rate monitoring during

labor were examined by a pediatric neurologist in the

neonatal period and then were subsequently evaluated

periodically (Table 7-10).188,244,246-248 Thirty-eight of

TABLE 7-10



Neonatal Neurological Course and

Subsequent Development in

Electronically Monitored Infants

FETAL HEART RATE PATTERNS*



Time of

Evaluation

Neonatal

(48-72 hr)

1 yr

6-9 yr

*



Normal



Moderate to

Severe Variable

Decelerations



Severe Variable

and/or Late

Decelerations



16%*

0%

0%



63%

6%

0%



73%

27%

10%



Percentage of patients with fetal heart rate pattern and abnormal

neurological evaluation.