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OBSTETRICS

Neonatal encephalopathy and the association

to asphyxia in labor
Maria Jonsson, MD, PhD; Johan Agren, MD, PhD; Solveig Norden-Lindeberg, MD, PhD;
Andreas Ohlin, MD, PhD; Ulf Hanson, MD, PhD
OBJECTIVE: In cases with moderate and severe neonatal encephalopathy, we aimed to determine the proportion that was attributable to
asphyxia during labor and to investigate the association between
cardiotocographic (CTG) patterns and neonatal outcome.
STUDY DESIGN: In a study population of 71,189 births from 2
Swedish university hospitals, 80 cases of neonatal encephalopathy
were identified. Cases were categorized by admission CTG patterns
(normal or abnormal) and by the presence of asphyxia (cord pH,
<7.00; base deficit,
12 mmol/L). Cases with normal admission
CTG patterns and asphyxia at birth were considered to experience
asphyxia related to labor. CTG patterns were assessed for the 2 hours
preceding delivery.
RESULTS: Admission CTG patterns were normal in 51 cases (64%)

and abnormal in 29 cases (36%). The rate of cases attributable to

asphyxia (ie, hypoxic ischemic encephalopathy) was 48 of 80 cases

(60%), most of which evolved during labor (43/80 cases; 54%). Both
severe neonatal encephalopathy and neonatal death were more
frequent with an abnormal, rather than with a normal, admission CTG
pattern (13 [45%] vs 11 [22%]; P .03), and 6 [21%] vs 3 [6%];
P .04), respectively. Comparison of cases with an abnormal and a
normal admission CTG pattern also revealed more frequently observed
decreased variability (12 [60%] and 8 [22%], respectively) and more
late decelerations (8 [40%] and 1 [3%], respectively).
CONCLUSION: Moderate and severe encephalopathy is attributable to

asphyxia in 60% of cases, most of which evolve during labor. An

abnormal admission CTG pattern indicates a poorer neonatal outcome
and more often is associated with pathologic CTG patterns preceding
delivery.
Key words: admission CTG pattern, asphyxia, encephalopathy,
hypoxic, ischemic, labor, neonatal encephalopathy

Cite this article as: Jonsson M, Agren J, Norden-Lindeberg S, et al. Neonatal encephalopathy and the association to asphyxia in labor. Am J Obstet Gynecol
2014;211:667.e1-8.

oderate and severe neonatal encephalopathy (NE) in the term or

near-term neonate are associated with
adverse outcomes that include neonatal
death, cerebral palsy, epilepsy, and other
cognitive and behavioral problems.1-4
The cause of NE is heterogeneous, and
risk factors are likely to be different in
different populations. Perinatal asphyxia
has been demonstrated to be associated
strongly with encephalopathy (ie, hypoxic ischemic encephalopathy [HIE]),5
but the proportion of cases that arise in
labor has not been established. An

accurate diagnosis of asphyxia requires

umbilical artery blood gas and acid-base
assessment at the time of birth, and a
signicant metabolic acidemia implies
exposure to asphyxia.6
A normal cardiotocographic (CTG)
pattern at admission to the delivery ward
is considered to represent normal central
nervous fetal behavior and absence of
hypoxia,7,8 whereas an abnormal CTG
pattern at admission implies an ongoing
antenatal, possibly hypoxic, event.9-11
Not only neonates with low Apgar
scores9 and metabolic acidemia,12 but

From the Department of Womens and Childrens Health, Uppsala University, Uppsala (Drs Jonsson,
gren, Nordn-Lindeberg, and Hanson), and Department of Pediatrics, rebro University Hospital,
rebro (Dr Ohlin), Sweden.
Received March 24, 2014; revised April 26, 2014; accepted June 11, 2014.
Supported by the Swedish Society of Medicine (Grant number SLS-170221), the Uppsala-rebro
Research Council (Grant number RFR-218041), the Gillbergska Foundation, the Swedish National
Infant Foundation, and the Linna and Josef Carlssons Foundation.
The authors report no conict of interest.
Corresponding author: Maria Jonsson, MD, PhD. maria.jonsson@kbh.uu.se
0002-9378/$36.00  2014 Elsevier Inc. All rights reserved.  http://dx.doi.org/10.1016/j.ajog.2014.06.027

also cases with HIE,13 have reported high

incidences of abnormal admission CTG
patterns. A small study on NE and the
timing of hypoxic injury found an
abnormal admission CTG pattern in
31% of cases, with a trend towards worse
outcomes in cases related to obstetric
emergencies.13
Thus, to categorize NE cases according
to their admission CTG pattern and their
acid-base status at birth might be useful
in understanding the timing of perinatal
asphyxia in relation to labor and delivery.
This, in turn, may enable the early
identication of cases that potentially
would be avoidable by improved fetal
monitoring and/or management. Although many fetuses who later present
with encephalopathy will display CTG
pattern abnormalities before delivery,11,14
no specic CTG pattern has shown to be
predictive.
By categorizing cases by means of
admission CTG pattern and metabolic
acidemia at birth, we aimed to determine
the proportion of moderate and severe

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TABLE 1

Summary of maternal characteristics and data on labor and delivery

Neonatal encephalopathy
Cardiotocography admission pattern
All (n [ 80)

Characteristics
Age, ya
2a

Body mass index, kg/m

a

Height, cm

Primiparity, n (%)

Normal (n [ 51)

Abnormal (n [ 29)

P value

30  4

30  4

31  4

.29

27  6

26  5

28  6

.28

164  7

163  6

165  7

.26

47 (59)

34 (65)

13 (45)

.06

39  2

39  2

39  2

.51

Gestational length
41 weeks, n (%)

22 (28)

13 (26)

9 (31)

.63

Complication to the pregnancy, n (%)b

6 (8)

5 (10)

1 (4)

.29

11(14)

4 (8)

7 (24)

.04

Spontaneous labor onset, n (%)

62 (77)

44 (86)

18 (62)

.013

Not in labor at admission, n (%)

18 (22)

7 (14)

11 (38)

.013

8 (27)

< .001

Gestational length, wk

Previous cesarean delivery, n (%)

Not in labor at admission,

inductions excluded, n (%)

8 (27)

Induction of labor, n (%)

10 (13)

7 (14)

3 (10)

.95

Premature rupture of membranes, n (%)

13 (16)

9 (17)

4 (14)

.65

3 (4)

1 (2)

2 (7)

.26

Occiput posterior position, n (%)

Delivery, n (%)
Breech

6 (8)

5 (10)

1 (3)

.27

Vacuum

24 (30)

19 (37)

5 (17)

.06

35 (54)

12 (24)

23 (79)

< .001

13 (16)

7 (14)

6 (21)

.42

34 (43)

16 (31)

18 (62)

.01

Cesarean
Sentinel event, n (%)

Female sex, n (%)

Birthweight, g

3517  681

3595  686

3378  660

.22

3 (4)

1 (2)

2 (7)

.26

7 (8)

5 (9)

2 (7)

.66

Small for gestational age, n (%)

Large for gestational age, n (%)

a

Data are given as mean (standard deviation); b Preeclampsia, hypertension, diabetes mellitus, intrahepatic cholestasis; c Shoulder dystocia, abruption, uterine rupture, eclampsia, cord prolapse,
vasa previa bleeding; d Defined as more or less than 2 standard deviations (SD) of mean birthweight.

Jonsson. Neonatal encephalopathy and labor asphyxia. Am J Obstet Gynecol 2014.

NE cases that were attributable to

asphyxia events before or after hospital
admission and to assess the proportion
that had evolved during labor (intrapartum HIE). Further, we aimed to
investigate the association between
admission CTG patterns and neonatal
outcome.

M ATERIALS

AND

M ETHODS

We used a dataset from a previous study

that held maternal and neonatal data on
all cases with moderate or severe encephalopathy at
34 weeks of gestation

from a population of 71,189 births at 2

university hospitals in Sweden: Uppsala
for the years 2003-2010 and rebro for
1994-2010.15 Three experienced obstetricians and a neonatologist reviewed the
maternal (M.J., S.N-L., U.H.) and
neonatal (J..) charts. The local ethics
committee in Uppsala approved the
study.
Cases had moderate-to-severe encephalopathy (grades 2 and 3) as dened
by Sarnat and Sarnat16 and Levene
et al.17 For the study periods, 80 infants
were identied with moderate (n 56)

667.e2 American Journal of Obstetrics & Gynecology DECEMBER 2014

or severe (n 24) encephalopathy,

which indicated an overall incidence of
1.1 of 1000 infants. Infants with major
central nervous system congenital malformations and chromosomal abnormalities were excluded.
As part of routine care, admission
CTG pattern and analysis of umbilical
artery acid-base status at birth were
performed in all deliveries. The guideline of the International Federation of
Gynecology and Obstetrics was used for
CTG interpretation.18 A portion of the
guideline is available in the Appendix

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TABLE 2

Cardiotocographic patterns during the last 2 hours before delivery

Neonatal encephalopathy, n (%)
Cardiotocography admission pattern
Variable

All (n [ 57)

Normal (n [ 37)

Abnormal (n [ 20)

Pathologic

49 (86)

30 (81)

19 (95)

.15

Tachycardia

23 (40)

13 (35)

10 (50)

.27

Bradycardia
5 minutes

17 (29)

14 (38)

3 (15)

.07

Variable decelerations

22 (38)

14 (38)

8 (40)

.87

Severe variable decelerations

17 (29)

11 (29)

6 (30)

.98

9 (16)

1 (3)

8 (40)

< .001

Decreased variability

20 (35)

8 (22)

12 (60)

.004

Contractions >5/10 minutes

15 (26)

14 (38)

1 (5)

.01

Late decelerations

P value

Percentages are given of women in labor that was monitored with cardiotocography (n 57).
Jonsson. Neonatal encephalopathy and labor asphyxia. Am J Obstet Gynecol 2014.

(Supplementary Table). The NE cases

were categorized in 2 groups based on
the admission CTG pattern: normal or
abnormal. A normal CTG pattern had
normal baseline fetal heart rate (110150 beats/min), variability of 5-25
beats/min, at least 2 accelerations, and
no decelerations. An admission CTG
pattern that did not meet these criteria
was categorized as abnormal and,
thus, had a suspicious or pathologic
pattern.18 The admission test usually is
recorded during a 20- to 60-minute
period; if the criteria for a normal test
are not reached within that time, further
evaluation is required.
CTG tracings during the last 2 hours
of labor were assessed independently.18
A hyperactive contraction pattern was
dened as
6 contractions every 10
minutes for at least 20 minutes. The
authors (M.J., S.N-L., and U.H.) who
assessed the CTG tracings were blinded
to neonatal outcome through the addition of control CTG tracings (1:1) that
were taken from singleton term infants
with an Apgar score <7 at 5 minutes or
metabolic acidemia in the umbilical
artery at birth. If assessments were
different, a joint assessment by majority
was performed.
Cases were grouped into HIE or nonHIE, depending on the acid-base status
at birth. Cases related to HIE were those
with umbilical artery or arterial (<1

hour after birth) samples that displayed

metabolic acidemia (pH <7.00 and base
decit of
12 mmol/L). In 2 cases,
an umbilical artery sample was missing,
but the venous sample was considered
appropriate. HIE cases were further
divided into antepartum or intrapartum
HIE. Cases that were attributable to intrapartum HIE were those with labor
(spontaneous or induced) and a normal
admission CTG pattern, whereas antepartum HIEs were those without labor
and an abnormal admission CTG pattern. In 3 cases, no acid-base data could
be retrieved; therefore, these were excluded from this analysis.
Infant outcome data and death causes
were retrieved from follow-up records
at 24 months or later after delivery.
Neurologic impairment was predened
to cerebral palsy, epilepsy, and mental
retardation. Therapeutic hypothermia
after peripartum hypoxia-ischemia was
available routinely to all eligible cases
from year 2008 (n 9 cases).

Statistics
The Statistical Package for Social Sciences software (version 20.0 for Windows; SPSS Inc, Chicago, IL) was used
for statistical analyses. Data are reported
as mean (standard deviation) and median (interquartile range). The c2 test or
Fisher exact test was applied for group
comparisons, and the Mann-Whitney U

test or t test was used for continuous

variables. A probability value of < .05
was considered statistically signicant.

R ESULTS
Of 80 infants with moderate or severe
NE, 51 infants (64%) had a normal
admission CTG pattern, and 29 infants
(36%) had an abnormal admission CTG
pattern. In total, 48 infants (60%) had
metabolic acidemia at birth (overall
HIE incidence, 0.67/1000 infants). Of
the 48 cases, 43 cases had labor (spontaneous or induced); the number of infants with HIE that evolved during labor
was 43 of 80 (54%), which proved the
incidence of intrapartum HIE to be 0.6
of 1000 cases.
Maternal characteristics and data on
labor and delivery are presented in
Table 1. Most pregnancies were uncomplicated (92%), but a history of
previous cesarean delivery was more
frequent in cases with an abnormal
admission CTG pattern. Labor onset
was spontaneous in 77% of cases and
more often among cases with a normal
admission CTG pattern. Of cases with
an abnormal CTG pattern, 8 women
(27%) were not in labor at admission
but were scheduled for a visit because of
premature rupture of the membranes or
postterm pregnancy. Other women had
come because of abdominal pain, decreased fetal movements, or bleeding,

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FIGURE

Neonatal outcome

Data are given in relation to admission cardiotocographic (CTG ) pattern, hypoxic ischemic encephalopathy (HIE ), and outcome at long-time follow-up evaluation. Neonatal acid-base data were
missing in 3 cases. Values are given as number (%). The asterisk denotes a probability value of .045.
Jonsson. Neonatal encephalopathy and labor asphyxia. Am J Obstet Gynecol 2014.

and delivery was conducted because of

suspected fetal compromise. The mode
of delivery differed, with more vacuum
deliveries in cases with normal admission CTG patterns and more cesarean
deliveries in cases with abnormal admission CTG patterns. Female sex of the
neonate was more common (P < .01)
in cases with an abnormal admission
CTG pattern.
During the last 2 hours before delivery, 57 cases (71%) had available CTG
patterns of a quality that allowed interpretation. A summary is presented in
Table 2. A pathologic intrapartum CTG
pattern was assessed in 30 cases (81%)
with a normal admission CTG pattern
and in 19 cases (95%) with an abnormal
admission CTG pattern. Late decelerations and decreased variability were
signicantly more frequent in cases with
an abnormal, compared with a normal,

admission CTG pattern. There were no

differences in occurrence of tachycardia,
bradycardia, or variable decelerations.
Hyperactive uterine contractions appeared more often in cases with a normal
admission CTG pattern: 38% vs 5%
(P .02). There were no differences in
median (interquartile range) duration of
the following CTG patterns when the
cases with normal and abnormal admission CTG patterns were compared:
pathologic CTG pattern, 43 (28e71) vs
60 (25e120) minutes; tachycardia, 70
(55e90) vs 120 (60e120) minutes; variable decelerations, 45 (20e120) vs 35
(25e65) minutes; and late decelerations,
100 (100e100) vs 120 (37e120) minutes,
respectively. Patterns with decreased
variability had longer duration among
cases with abnormal admission CTG
patterns: 95 (31e120) vs 30 (20e60)
minutes (P .013).

667.e4 American Journal of Obstetrics & Gynecology DECEMBER 2014

The Figure depicts neonatal outcome

in relation to admission CTG pattern,
stratied depending on the presence of
metabolic acidemia at birth. Adverse
outcome was more prevalent in HIE
cases with an abnormal, than a normal,
admission CTG pattern (78% vs 48%,
respectively; P .045). Neonatal outcomes at delivery and at follow-up evaluation for all NE cases are described in
Table 3. Severe encephalopathy and
neonatal death were more common
in cases with abnormal admission CTG
pattern; moderate encephalopathy was
more prevalent in cases with asphyxia
that evolved during labor. Adverse
neonatal outcome at follow-up evaluation was similar (55%) in both groups.
In the 32 neonates without HIE or
with missing acid-base data, neuroimaging that was performed within the
rst postnatal week indicated a perinatal
hypoxic ischemic event in 13 neonates.
In 3 neonates, an older lesion was
implied (periventricular leukomalacia);
2 neonates were diagnosed with perinatal cerebral infarction. There were
isolated cases of meconium aspiration,
sepsis, fetal anemia, cord prolapse,
shoulder dystocia, and neuronal migration disorder. In 3 cases, no cause
could be found, even after thorough
investigations.

C OMMENT
In our cohort, 60% of cases of moderateto-severe NE were attributable to asphyxia, and most of them evolved during
labor. The cases with an abnormal CTG
pattern at admission had a higher rate of
adverse outcome compared with those
with a normal CTG pattern. An abnormal admission CTG pattern was also
associated more often with intrapartum
CTG patterns that contained late decelerations and a decreased variability.
Most pregnancies were uncomplicated
and had a spontaneous onset of labor.
Identication of at-risk fetuses in such a
low-risk population is a particularly
demanding task for clinical management.
The present study includes a unique
birth cohort with an almost uniform
access to acid-base data, which rendered
an objective verication of asphyxia
possible. Thus, we believe that the

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TABLE 3

Neonatal outcome at delivery and at follow up

Neonatal encephalopathy
Admission cardiotocographic pattern
P value

Variable

All

Normal

Abnormal

Neonatal outcome

n 80

n 51

n 29

62 (77)

41 (80)

21 (72)

.41

35 (44)

25 (49)

10 (34)

.21

Apgar score at 5 min, n (%)

<7
<4
a

Umbilical artery pH

7.05 (6.85e7.19)

7.08 (6.87e7.22)

6.95 (6.85e7.15)

.07

Metabolic acidemia, n (%)b

48 (60)

29 (57)

19 (65)

.45

Encephalopathy grade 2, n (%)

56 (70)

40 (78)

16 (55)

.03

Encephalopathy grade 3, n (%)

24 (30)

11 (22)

13 (45)

.03

Died in the neonatal period, n (%)

9 (11)

3 (6)

6 (21)

.04

Outcome at long-time follow up, n (%)

n 71

n 48

n 23

Adverse outcome

39 (55)

25 (52)

14 (61)

.36

Cerebral palsy

13 (16)

10 (19)

3 (10)

.43

2 (7)

.04

Epilepsy

2 (3)

Cerebral palsy and epilepsy

Mental retardation
c

Died after the follow-up time

a

19 (24)

13 (25)

6 (21)

.77

5 (6)

2 (4)

3 (10)

.17

4 (5)

2 (4)

2 (7)

.44

Values are given as median (interquartile range); b pH <7.00 and base deficit
12 mmol/L in umbilical artery or <1-hour postnatal age; c Overlap with epilepsy and mental retardation.

Jonsson. Neonatal encephalopathy and labor asphyxia. Am J Obstet Gynecol 2014.

proportion of NE cases that were

attributable to asphyxia (ie, HIE) to be
reasonably accurate. By analyzing admission CTG patterns and assuming a
normal registration to indicate absence
of fetal compromise, we could also estimate the proportion of HIE cases that
arose during labor. Another strength of
our study was that assessments of CTG
tracings were made by the reviewers
individually who were blinded to neonatal outcome. Further, the population
was derived from 2 tertiary delivery
centers within the same region, which
ensured uniformity in obstetric care.
The study was limited by its retrospective design. Identication of cases
was based on the diagnosis of NE and/or
related diagnoses. Although every effort
was made to ensure proper identication
of all infants with NE, it is still possible
that unidentied and/or misdiagnosed
cases exist. Also, NE is a multifactorial
syndrome, and the distribution of different causes and risk factors might vary

between populations and over time,

which would render comparison and
extrapolation of data invalid. During
the study period, changes were implemented in the clinical management of
HIE (therapeutic hypothermia) and also
in the use of neuroimaging (more frequent use of magnetic resonance imaging) that might have changed the
awareness of NE, its diagnostics, and
outcome.
Previously reported incidences of
moderate-to-severe NE from populationbased studies range from 1.6e4.0 per
1000 live births,19,20 and the incidence of
HIE ranges from 0.7e2.0 per 1000.19,21,22
None of these studies include umbilical
artery acid-base data. In our study, for
which umbilical artery acid-base data
were available, the incidence of moderateto-severe NE was 1.1 per 1000 births, and
the incidence of HIE was 0.67 per 1000
births. We estimated 54% of NE cases to
be attributable to HIE having evolved
during labor. This nding is in contrast to

previous estimates that have suggested

that only 15-30% of cases of NE are
associated with intrapartum hypoxiaischemia.3,5,23 Several infants without
metabolic acidemia at birth still demonstrated neuroimaging ndings that
were consistent with hypoxia-ischemia as
the main mechanism of injury. This
supports the notion of a perinatal
hypoxic-ischemic event with a putative
intrauterine recovery of any acid-based
disturbance before birth. Our results are
in agreement with more recent prospective cohort studies that evaluated cases
with neuroimaging and report that 80%
of infants with NE have had a hypoxic
injury near the time of birth.24,25
The incidence of an abnormal
admission test in an unselected population is 3-5%.10 An association with thick
meconium, acidemia at birth, and an
Apgar score of <7 at 5 minutes has been
reported.9,10 Consistent with a previous
study,13 approximately one-third of the
infants with NE demonstrated an

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abnormal admission CTG pattern in

our cohort. The possibility of the prevention of neonatal morbidity and death
in infants with an abnormal admission
CTG pattern is difcult to evaluate,
because the duration and cause of fetal
compromise is not known. Furthermore, these fetuses may be more vulnerable, and labor might aggravate the
risk of neonatal morbidity.26 Most fetuses also displayed metabolic acidemia,
which underlines the importance of an
active approach when a woman has an
abnormal CTG pattern. The nding of a
signicantly higher rate of cases with
severe encephalopathy and neonatal
deaths in this group indicates that the
hypoxic process was at an advanced stage
in a substantial number of cases.
Most importantly, cases with normal
admission CTG patterns offer an obvious
preventive opportunity. Previous studies
have suggested that suboptimal intrapartum care might contribute to labor
asphyxia.15,27-29 It has been shown that
failure to identify or respond to a pathologic CTG trace is common in NE
cases.15,23-25 The predictive value of
different CTG patterns to identify encephalopathy cases is low,14 although associations exist with late decelerations,14
decreased variability,11,14,30,31 and longer
duration of abnormal CTG patterns31,32
during labor. Late decelerations and
decreased variability also featured in our
study, particularly in cases with an
abnormal admitting CTG pattern, where
higher rates of neonatal morbidity and
mortality were found.
Given the low incidence of NE, efforts
to improve intrapartum care might not
impact readily on the outcome measures at hand. Nevertheless, some maternity units have reported a decline in
moderate-to-severe encephalopathy,21,33
and case auditing might still be a
powerful tool to identify areas for
improvement.
In conclusion, asphyxia is the main
cause of moderate-to-severe encephalopathy in our population, and the occurrence of asphyxia is related strongly
to labor. An abnormal admission CTG
pattern indicates a higher risk of neonatal death and/or adverse neurologic
outcome, particularly in cases with

ajog.org
metabolic acidemia at birth. Pregnancies
were uncomplicated, and labor onsets
were spontaneous for most women;
thus, cases were not identied according
to any prenatal characteristics, which
limited the opportunities for prevention
during pregnancy. Strategies for prevention should be focused on events
related to labor.
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A PPENDIX
SUPPLEMENTARY TABLE

International Federation of Gynecologists and Obstetricians guidelines for fetal monitoring

Definition of antepartum fetal cardiotocograms
1. Normal pattern
Baseline heart rate of 110-150 beats/min
Amplitude of variability of 5-25 beats/min
Absence of decelerations, except for sporadic mild decelerations of very short duration
Presence of
2 accelerations during a 10-minute period
2. Suspicious pattern
Baseline heart rate of 150-170 beats/min or 100-110 beats/min
Amplitude of variability of 5-10 beats/min for >40 minutes
Absence of accelerations for >40 minutes
Sporadic decelerations of any type unless severe
3. Pathologic pattern
Baseline heart rate of <100 or >170 beats/min
Persistence of a heart rate variability of <5 beats/min for >40 minutes
Periodically recurring and repeated decelerations of any type
Sporadic and nonrecurrent decelerations of the following types: severe variable decelerations, prolonged decelerations, late decelerations
A sinusoidal pattern
Definition of intrapartum fetal cardiotocogram
1. Normal pattern
Baseline heart rate of 110-150 beats/min
Amplitude of variability of 5-25 beats/min
2. Suspicious pattern
Baseline heart rate of 150-170 beats/min or between 100-110 beats/min
Amplitude of variability of 5-10 beats/min for >40 minutes
Increased variability of >25 beats/min
Variable decelerations
3. Pathologic pattern
Baseline heart rate <100 or >170 beats/min
Persistence of a heart rate variability of <5 beats/min for >40 minutes
Severe variable decelerations or severe repetitive early decelerations
Prolonged decelerations
Late decelerations
A sinusoidal pattern
Suspicious or pathologic cardiotocographic patterns require conservative measures followed by fetal scalp sampling or delivery as appropriate.
Full guideline: Rooth G, et al.18
Jonsson. Neonatal encephalopathy and labor asphyxia. Am J Obstet Gynecol 2014.

667.e8 American Journal of Obstetrics & Gynecology DECEMBER 2014