Intrapartum Asphyxia, Neonatal Encephalopathy, Cerebral Palsy, and Obstetric

Interventions in the Term and Near-Term Infant

Shannon M. Clark, Sanmaan K. Basraon and Gary D.V. Hankins
Neoreviews 2013;14;e13
DOI: 10.1542/neo.14-1-e13

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Article

neurologic disorders

Intrapartum Asphyxia, Neonatal

Encephalopathy, Cerebral Palsy, and
Obstetric Interventions in the Term
and Near-Term Infant
Shannon M. Clark, MD,
Sanmaan K. Basraon, MD,

Abstract

Gary D.V. Hankins, MD

Intrapartum asphyxia (IA) as a cause of neonatal encephalopathy (NE) and cerebral

palsy (CP) is a concern for obstetric providers due to the signicant neonatal sequelae
that ensue. CP is a nonprogressive static neuromuscular disorder appearing early after
birth that occurs in 2 per 1,000 births. NE is a clinical syndrome of disturbed neurologic function in the rst week after birth, and it occurs in 6 per 1,000 live births.
Only w6% of all term infants diagnosed with CP have a history of NE, and without
the development of NE, IA cannot be considered as the sole cause of CP. There are
various preconceptional, antepartum, and intrapartum risk factors associated with CP.
Obstetric interventions, including various modalities of fetal monitoring and cesarean
delivery, have not led to improvement in outcomes or a reduction in the incidence of
CP. The goal of this review was to discuss the association of IA with NE and CP in
term and near-term infants, with a focus on the diagnosis and risk factors for IA and
potential obstetric interventions.

Author Disclosure
Drs Clark, Basraon,
and Hankins have
disclosed no financial
relationships relevant
to this article. This
commentary does
contain a discussion of
an unapproved/
investigative use of
a commercial product/

Objectives

After completing this article, readers should be able to:

1. Differentiate between cerebral palsy, neonatal encephalopathy, and intrapartum

asphyxia.
2. Define the criteria required to diagnose intrapartum asphyxia as a cause of moderate
to severe neonatal encephalopathy.
3. Identify preconceptional, antepartum, and intrapartum risk factors for the
development of neonatal encephalopathy and/or cerebral palsy.
4. Recognize potential obstetric interventions.

device.

Introduction

Abbreviations:
CD:
CNS:
CP:
EFM:
HIE:
IA:
NE:
SE:

cesarean delivery
central nervous system
cerebral palsy
electronic fetal monitoring
hypoxic-ischemic encephalopathy
intrapartum asphyxia
neonatal encephalopathy
sentinel event

In the majority of the cases of cerebral palsy (CP), the timing

of insult is largely unknown, and an isolated intrapartum
event causing asphyxia is rarely the cause of neurologic damage. It is prudent to understand the risk factors associated
with the development of intrapartum asphyxia (IA) and
the pathophysiology behind the development of neonatal
encephalopathy (NE) and CP. Currently, there is a dearth
of obstetric interventions that decrease the incidence of
these disorders; thus, further research is needed to develop
preventive strategies and targeted interventions aimed at improving neonatal outcomes. The goal of this review was to
discuss the association of IA with NE and CP in term and

University of Texas Medical Branch, Galveston, TX.

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neurologic disorders

intrapartum asphyxia

near-term infants, with a focus on the diagnosis and risk

factors for IA and potential obstetric interventions.

The Connection
Definition and Incidence
CP is dened as a nonprogressive static neuromuscular
disorder characterized by an abnormal control of movement or posture appearing early in life. (1) The onset occurs no later than age 1 year, and the denitive diagnosis
is typically reserved until age 4 to 5 years. The prevalence
of CP is w2 per 1,000 live births. Although term infants
are at relatively low risk for CP, approximately one half of
all births with CP are term and near-term infants (2) as
term births constitute about 92% of all births. Whereas
CP has many causes that may or may not be recognized
at birth, NE is recognizable at birth.
NE is a clinically dened syndrome of disturbed neurologic function manifested by difculty with initiating and
maintaining respirations, depression of tone and reexes,
altered level of consciousness, and often seizures in the rst
week after birth in the near-term and term infant. (3)(4)(5)
(6) Such acute neonatal neurologic dysfunction is the earliest and best indicator of neurologic injury and increased
risk for later neurodevelopmental sequelae. (7) NE occurs
in 1 to 6 per 1,000 live term births, (2) with 15% to 20% of
affected newborns dying in the postnatal period and an
additional 25% sustaining childhood disabilities. (8)
IA is a known cause of NE. A key feature in the consideration of IA as a cause of CP in an individual infant is
the concomitant presence of symptoms of moderate to
severe NE. However, only 6% of all term infants diagnosed with CP have a history of NE; (9) therefore, the
great majority of term CP cannot be considered to be
the result of an intrapartum injury. (10) The reported incidence of IA in term or near-term infants is 1 to 8 neonates per 1,000 live term births, with 0.5 to 1.6 per 1,000
subsequently developing NE. (11) Of those with NE due
to IA, between 10% and 60% will die, and w25% of the
survivors will have long-term neurodevelopmental sequelae. (4) Other investigators (6)(7)(8)(9)(10)(11)
(12) have reported that only 8% to 15% of term infants
with NE, and even fewer with early neonatal seizures,
(13) have evidence of asphyxia immediately before birth.
Finally, IA as a cause of CP occurs in only a minority of
cases and has been cited as low as 10% and as high as 20%.
(14)(15)

Timing of Injury
Even though guidelines for diagnosing IA as a cause of
NE have been established, determining if asphyxia was

present before the onset of labor or developed during

labor and delivery is difcult to ascertain. In addition,
intrapartum adverse events could be the result of an antepartum predisposition or antepartum onset of brain injury or brain dysfunction that results in a negative
response of the fetus to the stresses incurred during labor
and delivery. (16)(17) As such, difculties during the
course of labor and delivery could be secondary to fetal
compromise predating labor, and subsequent poor oxygenation or fetal hypotension during labor are merely
contributors to the development of NE. (17) However,
even if antenatal factors are identied, it is still difcult to
prove that subsequent injury did not occur during the
intrapartum period.
The Western Australian case-control study by Badawi
et al (4) in 1998 compared 164 term infants exhibiting
moderate to severe NE (broadly dened) with 400 randomly selected controls. They found no evidence of intrapartum hypoxia in more than 70% of NE cases, and
isolated IA accounted for only 4% of moderate to severe
NE. Furthermore, they noted that most causes of NE
were heterogeneous and most commenced in the antenatal period. These ndings were in agreement with an international consensus statement, which noted that
epidemiologic studies suggest that w90% of cases of
CP have no history of IA. (18) In the remaining 10%,
intrapartum signs compatible with damaging hypoxia
may have had either antenatal or intrapartum origins.
However, there are conicting reports that suggest otherwise. In 2003, Cowan et al (19) used neonatal brain
magnetic resonance imaging or postmortem examination
in 351 term infants with NE, early seizures, or both to
distinguish between lesions acquired antenatally and
those that developed in the intrapartum and early postpartum period. They found that greater than 90% of term
infants with NE, seizures, or both, but without specic
syndromes or major congenital defects, had evidence of
perinatally acquired insults, and there was a very low rate
of established brain injury acquired before birth.
However, their data could not exclude the possibility
that antenatal factors might contribute to perinatal brain
injury and, in addition to genetic predispositions to
hypoxic-ischemic injury, may render the fetus more susceptible to the stresses of labor and delivery.

Clinical Criteria for Diagnosing Intrapartum

Asphyxia
Pathophysiology of Intrapartum Asphyxia
The diagnosis of IA (fetal hypoxia and/or ischemia) includes impaired respiratory gas exchange and development

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neurologic disorders

of fetal metabolic acidosis (20) during labor and delivery

with oxygen deprivation in fetal brain either through
hypoxia and/or ischemia. Hypoxemia results from diminished oxygen in the fetal blood supply, and cerebral
ischemia occurs due to impaired blood supply to the fetal
brain, with the latter resulting in deprivation of glucose,
which further contributes to the development of neuronal injury. (21) When an intrapartum insult occurs as a result of various events, the placental blood ow and gas
exchange is impaired, leading to a cycle of ischemia
and reperfusion of the fetal brain that results in necrosis
and cell death. (22)(23) After such insult, the fetal cardiac
output is redistributed, with decreased blood ow to the
lungs, kidney, and intestine with preservation of circulation to the brain, heart, and adrenals. (24)
Of utmost importance is the maintenance of the integrity of the central nervous system (CNS), especially the
brain, during the compensatory phase of an asphyxial
exposure that is accomplished by a combination of increased cerebral blood ow and oxygen extraction.
(24) Damage is greatest when the asphyxial exposure persists and cardiovascular decompensation occurs. A severe
metabolic acidosis then develops, and the combination of
asphyxia and ischemia due to hypotension and hypoperfusion results in a decrease in cerebral oxygen consumption and ultimately brain injury and end-organ damage.
(24) A fetus can usually compensate and recover after
an asphyxial exposure with correction of respiratory acidosis. (25) However, recurrent, intermittent, or continuous asphyxial insults causing metabolic acidosis for
a prolonged period of time can result in varying degrees
of brain injury depending on the gestational age of the
fetus. Ultimately, these events can lead to short-term
sequelae, as represented by NE, or long-term sequelae,
as seen with CP.

Clinical Diagnosis of Intrapartum Asphyxia

Currently, the standard for dening an acute intrapartum
hypoxic-ischemic event as sufcient to cause moderate to
severe NE in term and near-term neonates that subsequently results in CP uses the four essential criteria put
forth by the American College of Obstetricians and Gynecologists and American Academy of Pediatrics Task
Force on Neonatal Encephalopathy and Cerebral Palsy
(Table 1). (26) If all of these criteria are met, it is likely
that the pathology causing CP occurred during labor.
The task force also presented ve criteria that suggest
an intrapartum timing of a hypoxic event within 48 hours
of delivery when present collectively but are nonspecic
to asphyxial insults. These criteria are weakly associated
with an acute IA event, with the exception of the rst

intrapartum asphyxia

one (a sentinel or hypoxic event occurring immediately

before or after the onset of labor). (3)
Even when all four essential criteria are met, the timing of the insult cannot be denitely determined.
Hypoxia could be intermittent, chronic, or acute during
labor in a previously healthy fetus. However, if an ischemic cerebral injury occurred in the intrapartum period,
results of the neurologic examination of the neonate will
be abnormal within the rst 24 hours of birth. Abnormalities can be observed in the following: 1) cortical function
(lethargy, stupor, coma with or without seizures); 2)
brainstem function (pupillary and cranial nerve abnormalities); 3) tone (hypotonia); and 4) reexes (absent,
hyporeexia). (7(21) If the NE that develops after an
IA event is severe enough to cause CP, it is of the spastic
quadriplegic or dyskinetic type. (3)(27)(28) Unilateral
brain lesions, hemiparetic CP, (29)(30) hemiplegic CP,
spastic diplegia, and ataxia have not been associated
with acute IA. (30) Finally, any progressive neurologic
disability is not CP and thus not a result of an acute IA
event. (3)
When considering fetal tracings, abnormal patterns
most frequently found to be associated with the development of CP include multiple late decelerations and
decreased beat-to-beat variability. (3) Of note, the presence of such tracings may be the rst sign of a pre-existing
fetal neurologic abnormality, (31) severe antenatal neurologic injury, (32)(33) or an acute intrapartum injury.
However, there is a high false-positive rate when predicting CP. (34) Nelson et al (34) found that intrapartum
fetal heart rate tracing abnormalities as a marker for IA
had poor predictive value for the development of NE;
the presence of multiple late decelerations and/or persistent decreased beat-to-beat variability had a false-positive
predictive rate for subsequent development of CP of
99.8%. Similarly, it is known that 1- or 5-minute Apgar
scores alone are poor predictors of long-term neurologic
outcome, with 75% of children with CP obtaining normal
Apgar scores at birth. (35) Finally, extremely low Apgar
scores at 15 and 20 minutes only have been shown to
strongly correlate with subsequent neurologic dysfunction. (3)
The best indicator for IA is metabolic acidosis (pH <7
and base decit 12 mmol/L) in umbilical arterial blood
at the time of delivery. (18)(36) This nding allows for an
accurate diagnosis of asphyxia via umbilical cord blood
gas and acid base assessment. (24) It is recommended
that both arterial and venous cord blood be obtained because arterial blood reects fetal status more directly and
venous blood reects whether the uteroplacental oxygen
exchange is optimal; (37) however, this testing is not
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neurologic disorders

intrapartum asphyxia

Criteria for Defining an Acute Intrapartum Hypoxic-Ischemic

Event as a Cause of CP (26)

Table 1.

Essential Criteria

Suggestive Criteria

Evidence of metabolic acidosis in fetal umbilical cord

arterial blood at delivery (pH <7 and base deficit 12
mmol/L)
Early onset of severe or moderate neonatal
encephalopathy in infants born after 34 weeks
gestation

A sentinel or hypoxic event occurring immediately before

or after the onset of labor

CP of the spastic quadriplegic or dyskinetic type

Exclusion of other identifiable causes

Sudden and sustained fetal bradycardia or the absence of

fetal heart rate variability in the presence of persistent,
late, or variable decelerations after a previously normal
fetal heart rate pattern
Apgar scores of 03 beyond 5 min
Onset of multisystem organ involvement within 72 h of
delivery
Early imaging showing evidence of acute nonfocal
cerebral abnormality

CPcerebral palsy.

always feasible. If there is signicant metabolic acidosis at

the time of sampling, it is likely that IA has occurred.
However, it does not indicate the duration of exposure
or whether it was continuous or intermittent. (24) The
diagnosis of IA is based on the presence of metabolic
acidosis; the severity of the asphyxia is based on the degree of NE and the presence of other organ system complications. (24)
Multisystem organ involvement, once thought to be
a requirement for the diagnosis of IA, was included on
the list of nonspecic criteria for hypoxic-ischemic encephalopathy (HIE) by the American College of Obstetricians and Gynecologists/American Academy of
Pediatrics Task Force. (26) As previously mentioned,
during an IA event, an attempt is made to preserve perfusion to the vital organs by shunting blood away from
other organ systems. (11) As a result, elevation in liver
enzyme levels, impaired renal function and acute tubular
necrosis, and heart injury may be observed in the neonate. Laboratory assessment should occur as soon as possible after delivery if IA is believed to be present, and
followed over the next several days to weeks because
some markers do not immediately appear as abnormal.
In a 2002 study by Hankins et al, (38) 46 cases of
acute peripartum asphyxia sufcient to result in the diagnosis of NE were identied through a prospectively maintained database. Using criteria to dene an acute IA event
that are slightly different from what is used today, the authors identied how often various organ systems reected
injury patterns by using commonly available laboratory
tests and/or imaging technologies. They included patients with an obvious acute intrapartum event of recent

onset, such as a placental abruption, umbilical cord prolapse, or deterioration in a previously normal fetal heart
rate pattern in gestations greater than 32 weeks. They
found that in cases with clinical CNS injury resulting in
encephalopathy, 49% had abnormal results on electroencephalogram and 40% had imaging studies that were diagnostic of acute injury. In addition, liver injury, based on
elevated transaminase levels, occurred in 80%; heart injury, as dened by pressor or volume support beyond 2
hours after birth or elevated cardiac enzyme levels, occurred in 78%; and renal injury, dened by an elevation
of serum creatinine to greater than 1.0 mg/dL, persistent
hematuria, persistent proteinuria, or clinical oliguria,
occurred in 72%. Finally, when combining results of
laboratory and imaging studies, involvement of the renal,
hepatic, CNS, and cardiac systems was observed in
greater than 70% of cases. Hankins et al concluded that
multiple organs suffer damage during an acute IA event
sufcient to result in NE, and absence of injury does not
correlate with the diagnosis of IA.

Risk Factors
Preconceptional and Antepartum Risk Factors
There is a higher incidence of maternal illness, antenatal
complications, and adverse social factors in infants with
NE, seizures, or both, (2)(3)(5)(30)(39)(40)(41)(42)
(43)(44) most occurring occur well before birth, which
must be excluded before the diagnosis of IA is made.
(19)(26) As previously discussed, the presence of antepartum risk factors may render the fetus more susceptible
to the stresses of labor and delivery, and further increase
the risk of IA. In this scenario, it is impossible to

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neurologic disorders

determine whether the antepartum risk factor(s) or an intrapartum insult played the key role in the development
of NE and/or CP. Conversely, the presence of antepartum risk factors does not mean that an acute intrapartum
event cannot occur.
In addition to intrapartum insults, Badawi et al, (5) in
their population-based unmatched case-control study of
term infants, found various preconceptional and antenatal factors that increase the risk of NE and/or CP as summarized in Tables 2 and 3. Various social factors, family
and personal history, and infertility treatment were
strongly associated with risk of development of NE
and/or CP. In addition, various antenatal factors, most
importantly maternal thyroid disease, severe preeclampsia, and intrauterine growth restriction (less than the third
percentile for birthweight), had a strong association with
NE. They concluded that there are numerous causes of
NE, many of which start before labor and delivery. In
2011, Maisonneuve et al (45) identied risk factors of
severe acidosis in a case-control study of term pregnancies
with severe neonatal acidosis (umbilical artery pH < 7.0)
and found severe acidosis in 0.63% of 39,321 live term
births. They did not use all criteria for the diagnosis of
IA for the purposes of this study. Maternal age greater
than 35 years, previous neonatal death and previous cesarean delivery (CD), were independent risk factors for
severe neonatal acidosis (Tables 2 and 3).
Chorioamnionitis (intrapartum maternal and/or fetal
tachycardia and maternal temperature elevation) increase
the risk of NE and CP. (2) Although chorioamnionitis is
readily identiable during the course of labor and delivery, other antepartum infections are variable in their sequelae and ease of diagnosis. It is well known that
rubella and cytomegalovirus are viral teratogens; however, there are other viruses that may play a role in fetal
neurologic damage in the antepartum period. (46) In addition, maternal hyperthermia, inammatory mediators,
and other pathophysiologic sequelae observed with any
maternal infection may contribute to the development
of IA and NE. (47) In the event that antenatal or intrapartum exposure to infection occurs, neonates should be
evaluated by using proper laboratory assessments and
examination, and, ideally, the placenta should be sent
for pathologic evaluation.

Intrapartum Risk Factors

A sentinel event (SE) is an acute intrapartum pathologic
event that causes neurologic damage to a previously intact fetus through compromised blood or oxygen supply.
(3) Although the task force considers it as a criterion suggestive of an IA event as a cause of NE, an SE is more

intrapartum asphyxia

strongly associated with acute IA than other criteria.

(26) Examples of SEs and intrapartum risk factors are
shown in Table 4. (2)(3)
A retrospective population-based study by Gilbert et al
(48) in 2010 examined adverse intrapartum events in children with spastic quadriplegic or dyskinetic type CP. These
events included abruption, uterine rupture, fetal distress,
birth trauma, prolapsed cord, and mild to severe birth asphyxia. The frequency of CP within the study population
was 1.4 per 1,000 deliveries. Overall, 31.3% of these children had one or more of the six adverse intrapartum events
compared with 12.9% of controls. Fifty-nine percent
(4,274 of 7,242) of children identied with CP in this
study were term births; 28.3% had one or more adverse
events compared with 12.7% in controls. The authors
noted that these ndings could show that birth-related
events are a more signicant cause of the development
of CP than previously thought. However, overall, the majority of children who had CP did not have an adverse intrapartum event related to their development of CP.
In a 2012 retrospective double cohort study of three
groups of infants at greater than 35 weeks gestation exposed to different risk factors for IA, Martinez-Biarge
et al (49) examined perinatal morbidity and the rate of
HIE in infants exposed to intrapartum SE. These groups
included the following: (1) infants with an intrapartum SE;
(2) infants delivered by emergency CD or operative vaginal delivery due to abnormal fetal heart rate tracing;
and (3) infants delivered by elective CD before the onset
of labor. SE included uterine rupture, placental abruption,
cord prolapse, and amniotic uid embolism. Diagnosis of
HIE was made when the infant met the criteria for neonatal depression/cord arterial pH 7.00 or Apgar score
3 at 1 minute and/or 5 at 5 minutes or need for advanced resuscitation; and NE as presented by Leviton
and Nelson. (6) They found that perinatal mortality was
6% in the SE group and 0.3% in the nonreassuring fetal
status group (relative risk [RR]: 2.4 [95% condence interval (CI): 1.952.94]) with perinatal morbidity increased
two to six times in infants exposed to SE. The incidence
of HIE was 10% in the SE group compared with 2.5%
in the nonreassuring fetal status group (RR: 1.93 [95%
CI: 1.492.52]). When considering SE, uterine rupture
was associated with the highest incidence of HIE (32%),
followed by placental abruption (11%). Finally, no infant
in the elective cesarean group died, had perinatal morbidity, or developed encephalopathy. The authors concluded
that intrapartum SE are a signicant cause of perinatal
morbidity and the development of HIE. (49)
The 1998 Australian study of Badawi et al (4) also examined various intrapartum predictors for NE in term
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neurologic disorders

intrapartum asphyxia

Preconceptional Risk
Factors for NE and/or CP

Table 2.

Risk Factor

OR (95% CI)

Increasing maternal age

35 y (5,45)
Social factors (5)
Unemployment
Unskilled manual worker
Housewife
No private health insurance
Family history (5)
Seizures
Neurologic disease
Infertility treatment (5)
Previous neonatal
deatha (45)
Previous CD even after
excluding uterine
rupturea (45)

6.01 (1.2828.15)/
5.58 (2.5112.40)a

identiable risk factors. They concluded that IA accounts

for a small proportion of cases of NE, and elective CD has
an inverse association with NE.

Obstetric Interventions
Electronic Fetal Monitoring

For the term and near-term infant, the most obvious

3.60 (1.1011.80)
tool that the obstetrician can use to identify fetuses at
3.84 (1.4310.28)
risk for IA and decrease the risk of intrapartum fetal
2.48 (1.145.39)
3.46 (1.259.59)
death or neonatal seizures is electronic fetal monitoring
(EFM) during labor and delivery. (50) Although some
2.55 (1.314.94)
studies report that EFM correlates with the onset of
2.73 (1.166.41)
metabolic acidosis and subsequent neurologic injury,
4.43 (1.1217.60)
(50)(51) there is no consensus on this subject, and investigators disagree on what is the most ominous fetal
4.08 (1.719.72)a
heart rate pattern that signies potential metabolic acidosis. In general, prolonged decreased variability with
repetitive, prolonged late or variable decelerations and
CIcondence interval, CPcerebral palsy, NEneonatal
sustained bradycardia are all potential signs of impendencephalopathy, ORodds ratio.
a
ing neonatal metabolic acidosis. In general, however,
Denotes risk factors for neonatal acidosis.
the predictive power of EFM for the development of
NE and CP is low, (25) and to date, the use of EFM
has not decreased the incidence of CP. (52) This is likely
due to the fact that most cases of CP are a result of
infants (Table 4). They found that the prevalence of
events that occurred before the onset of labor, and a very
moderate or severe NE was 3.8 per 1,000 term live births
small percentage of cases are a result of IA. (3)(5) Overwith a neonatal mortality rate of 9.1%. When considering
all, EFM has led to an increase in obstetric interventions
risk factors, 69% of case infants had only antepartum risk
in the form of cesarean and operative vaginal deliveries,
factors for NE, 24% had antepartum and intrapartum facespecially during active labor. (53) This affords the potors, 5% had only intrapartum factors, and 2% had no
tential for increased complications for both the mother
and fetus. Despite this risk, EFM is
the best tool obstetricians can use in
Table 3.
labor in an effort to identify fetal
metabolic acidosis.
Risk Factor
Adjusted OR (95% CI)
ST waveform analysis includes the
addition of the fetal electrocardioViral illness: 2.97 (1.525.80)
Maternal prothrombotic disorders and
proinflammatory states (ie, intrauterine
gram to standard cardiotocography
infections, maternal infectious disease,
for intrapartum fetal monitoring in
viremia) (5)
an attempt to reduce neonatal and feCongenital malformations (2)
tal asphyxia. (54)(55) A metaChromosomal/genetic abnormalities (43)
analysis of randomized controlled
Maternal thyroid disease(5)
9.7 (1.9747.91)
Severe preeclampsia(5)
6.3 (2.2517.62)
trials by Becker et al (56) in 2012
Intrauterine growth restriction (5)(39)(40)(44)
38.23 (9.44154.76) for
compared the effects on ST wave<3rd percentile for
form analysis with standard continbirthweight
uous cardiotocography in singleton
Trauma (3)
pregnancies in cephalic presentation
Multiple gestation (3)
Antepartum hemorrhage (moderate or severe) (5) 3.57 (1.309.85)
at 34 weeks gestation. They evalBreech presentation (3)
uated various abnormalities in metabolic acidosis, umbilical cord pH,
CIcondence interval, CPcerebral palsy, NEneonatal encephalopathy, ORodds ratio.
Apgar scores, admittance to the

Antepartum Risk Factors for NE and/or CP

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neurologic disorders

Intrapartum Risk Factors and Sentinal

Events (*) for NE and/or CP

Table 4.

Risk Factor

Adjusted OR (95% CI)

a

Abnormal fetal heart rate during labor (45) (ie,

severe and sustained bradycardia, absent variability,
persistent late or variable decelerations)
Thick meconiuma (45)
Chorioamnionitis/maternal fever (4)
Persistent occipito-posterior position (4)
Operative vaginal delivery (4)
General anesthesiaa (45)
Emergency CD (4)
Uterine rupture* (26)(45)
Placental abruption* (26)
Maternal cardiac arrest* (26)
Amniotic fluid embolus* (26)
Umbilical cord prolapse* (26)
Fetal exsanguination* (26) (ie, vasa previa, massive
fetomaternal hemorrhage)

8.77 (3.7220.78)
5.81
3.82
4.29
2.34
8.04
2.17

(1.7219.66)
(1.4410.12)
(1.7410.54)
(1.164.70)
(1.2650.60)
(1.014.64)

intrapartum asphyxia

intrapartum risk factors rather than

bypassing the potential for adverse
intrapartum events. (4) Currently,
there is no recommendation for the
performance of elective CD for the
prevention of IA and the subsequent
development of NE and CP.

Other Interventions

One of the most obvious interventions obstetricians have is antenatal

screening for the detection of risk
factors for adverse antepartum
and intrapartum outcomes. (25)
Early detection allows earlier intervention and informed decisionmaking regarding mode and timing
of delivery. Identication of maternal and fetal disease is of utmost imCDcesarean delivery, CIcondence interval, CPcerebral palsy, NEneonatal encephalopathy,
portance. When considering labor
ORodds ratio.
a
and delivery, there are several interDenotes risk factors for neonatal acidosis; * Denotes sentinal events for NE and/or CP.
ventions that obstetricians use
when faced with a nonreassuring
fetal heart tracing. These interventions include maternal oxygen supNICU, need for intubation, presence of HIE, perinatal
plementation and position change, tocolytic agents (ie,
death, operative delivery, and number of fetal blood
b2-adrenergic agonist), and amnioinfusion. In some of
samplings. They found that ST waveform analysis did
these cases, these measures allow resuscitation before
not reduce the occurrence of metabolic acidosis (RR:
the decision is made to proceed with CD.
0.72 [95% CI: 0.431.19]). However, ST waveform
analysis did signicantly reduce the incidence of additional fetal blood sampling (RR: 0.59 [95% CI: 0.44
American Board of Pediatrics NeonatalPerinatal
0.79]), operative vaginal deliveries (RR: 0.88 [95% CI:
Content Specifications
0.800.97]), and total operative deliveries (RR: 0.94
[95% CI: 0.890.99]). (56) Although fetal blood sam Know the clinical features, diagnosis, and
pling is not standard practice in most institutions, conmanagement of perinatal hypoxicischemic encephalopathy.
tinuous cardiotocography for intrapartum fetal

Differentiate asphyxia from other causes

monitoring is still used. Trials are underway to deterof depression at birth, including drug
mine if ST waveform analysis is effective in reducing
effects and hypovolemia.
the occurrence of neonatal metabolic acidosis.
Understand the significance, limitations, and causes of low

Cesarean Delivery
CD has well-known surgical risk to the mother, especially
with subsequent repeat CD. When considering the term infant and CD, the risk of respiratory complications is greater,
especially in the case of elective CD in the absence of labor.
There is evidence that CD for the breech fetus reduces perinatal mortality, neonatal mortality, and serious neonatal
morbidity with a planned CD. (57) Although it seems reasonable that elective CD may decrease the incidence of IA,
any benet may indeed be due to avoidance of certain

Apgar scores.
Know the interpretation of fetal scalp and umbilical cord
blood gas and pH values.
Know the approximate risk of cerebral palsy in very low
birthweight, moderately low birthweight, and normal
birthweight infants.
Know the relationship between Apgar scores and later
development of cerebral palsy in preterm and term infants.
Know the prenatal, perinatal, and neonatal risk factors for the
development of cerebral palsy.
Know that the majority of children with cerebral palsy have
no identifiable cause.

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neurologic disorders

intrapartum asphyxia

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Intrapartum Asphyxia, Neonatal Encephalopathy, Cerebral Palsy, and Obstetric

Interventions in the Term and Near-Term Infant
Shannon M. Clark, Sanmaan K. Basraon and Gary D.V. Hankins
Neoreviews 2013;14;e13
DOI: 10.1542/neo.14-1-e13

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