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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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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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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, 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 nancial relationships relevant to this article. This commentary does contain a discussion of an unapproved/ investigative use of a commercial product/ device.


After completing this article, readers should be able to:

1. Differentiate between cerebral palsy, neonatal encephalopathy, and intrapartum asphyxia. 2. Dene 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.

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

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

University of Texas Medical Branch, Galveston, TX.

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near-term infants, with a focus on the diagnosis and risk factors for IA and potential obstetric interventions.

The Connection
Denition 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)

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

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

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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Table 1.

Criteria for Dening an Acute Intrapartum Hypoxic-Ischemic Event as a Cause of CP (26)

Essential Criteria Evidence of metabolic acidosis in fetal umbilical cord arterial blood at delivery (pH <7 and base decit 12 mmol/L) Early onset of severe or moderate neonatal encephalopathy in infants born after 34 weeks gestation CP of the spastic quadriplegic or dyskinetic type Exclusion of other identiable causes Suggestive Criteria A sentinel or hypoxic event occurring immediately before or after the onset of labor 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
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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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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

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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Table 2.

Preconceptional Risk Factors for NE and/or CP

Risk Factor 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) OR (95% CI) 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 proinammatory 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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Table 4.

Intrapartum Risk Factors and Sentinal Events (*) for NE and/or CP

Risk Factor 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 uid embolus* (26) Umbilical cord prolapse* (26) Fetal exsanguination* (26) (ie, vasa previa, massive fetomaternal hemorrhage)

Adjusted OR (95% CI) 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 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 Specications 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 signicance, 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 identiable cause.

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1. Aisen ML, Kerkovich D, Mast J, et al. Cerebral palsy: clinical
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