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The American College of Obstetricians and Gynecologists (ACOG) convened a Task Force on Neonatal Encephalopathy and Cerebral Palsy to collate and review the best scientific data available on the topic and to publish these findings. The American Academy of Pediatrics collaborated with ACOG on the Task Force and is a co-author of the final report. This executive summary covers important information and is intended to complement, not substitute, the full report.

Neonatal encephalopathy and its subset of hypoxic-ischemic encephalopathy (HIE) are conditions defined in and described for term and near-term infants. Neonatal encephalopathy is defined clinically on the basis of a constellation of findings to include a combination of abnormal consciousness, tone and reflexes, feeding, respiration, or seizures and can result from myriad conditions. Neonatal encephalopathy may or may not result in permanent neurologic impairment. It can be stated with certainty, however, that the pathway from an intrapartum hypoxic-ischemic injury to subsequent cerebral palsy must progress through neonatal encephalopathy.

In contrast, cerebral palsy is a chronic disability of central nervous system origin characterized by aberrant control of movement and posture, appearing early in life and not as a result of progressive neurologic disease. Research supports that spastic quadriplegia, especially with an associated movement disorder, is the only type of cerebral palsy associated with an acute interruption of blood supply. Purely dyskinetic or ataxic cerebral palsy, especially where there is an associated learning difficulty, commonly has a genetic origin and is not caused by intrapartum or peripartum asphyxia. Similarly, absent cerebral palsy, neither epilepsy, mental retardation, nor attention-deficit hyperactivity disorder are caused by birth asphyxia.

Historically, the factors used to define perinatal asphyxia, such as meconium-stained amniotic fluid and Apgar scores, were not specific to the disease process leading to neurologic damage. For instance, Nelson and associates have shown that use of nonreassuring fetal heart rate patterns to predict subsequent cerebral palsy had a 99% false-positive rate. Use of such nonspecific markers for perinatal asphyxia identifies a large number of individuals as being exposed to inappropriately diagnosed "perinatal asphyxia." Thus, it is not surprising that removing exposure to such nonspecific markers has failed to change the risk for the disease.

Epidemiologic studies have shown that only 19% of cases of neonatal encephalopathy met what were very nonstringent criteria for intrapartum hypoxia, with another 10% experiencing a significant intrapartum event that may have been associated with intrapartum hypoxia. Even with such inexact markers for intrapartum fetal hypoxia, they demonstrated that of all cases of neonatal encephalopathy, 69% had only antepartum risk factors, 25% had both antepartum and intrapartum risk factors, 4% had evidence of only intrapartum hypoxia without identified preconceptional or antepartum factors that might have contributed to neonatal encephalopathy, and 2% had no identified risk factors. Thus, approximately 70% of neonatal encephalopathy is secondary to events arising before the onset of labor. The overall incidence of neonatal encephalopathy attributable to intrapartum hypoxia, in the absence of any other preconceptional or antepartum abnormalities, is estimated to be approximately 1.6 per 10,000. It is again emphasized that HIE is but one subset of neonatal encephalopathy; other subsets include those resulting from prenatal stroke, infection, cerebral malformation, genetic disorders, and many other conditions.

The criteria to define an acute intrapartum event sufficient to cause cerebral palsy, as modified by this Task Force from the template provided by the International Cerebral Palsy Task Force, are listed as follows:*

Essential criteria (must meet all four)

1. Evidence of a metabolic acidosis in fetal umbilical cord arterial blood obtained at delivery (pH <7 and base deficit =12 mmol/L)
2. Early onset of severe or moderate neonatal encephalopathy in infants born at 34 or more weeks of gestation
3. Cerebral palsy of the spastic quadriplegic or dyskinetic type†
4. Exclusion of other identifiable etiologies such as trauma, coagulation disorders, infectious conditions, or genetic disorders

Criteria that collectively suggest an intrapartum timing (within close proximity to labor and delivery, eg, 0-48 hours) but are nonspecific to asphyxial insults

1. A sentinel (signal) hypoxic event occurring immediately before or during labor
2. A sudden and sustained fetal bradycardia or the absence of fetal heart rate variability in the presence of persistent, late, or variable decelerations, usually after a hypoxic sentinel event when the pattern was previously normal
3. Apgar scores of 0-3 beyond 5 minutes
4. Onset of multisystem involvement within 72 hours of birth
5. Early imaging study showing evidence of acute nonfocal cerebral abnormality

*Modified from MacLennan A. A template for defining a casual relation between acute intrapartum events and cerebral palsy: international consensus statement. BMJ 1999;319:1054-9. †Spastic quadriplegia and, less commonly, dyskinetic cerebral palsy are the only types of cerebral palsy associated with acute hypoxic intrapartum events. Spastic quadriplegia is not specific to intrapartum hypoxia. Hemiparetic cerebral palsy, hemiplegic cerebral palsy, spastic diplegia, and ataxia are unlikely to result from acute intrapartum hypoxia (Nelson KB, Grether JK. Potentially asphyxiating conditions and spastic cerebral palsy in infants of normal birth weight. Am J Obstet Gynecol 1998;179:507-13).

The Task Force recognizes that this summary will require updating as the scientific database and knowledge on this topic expands. Only with more complete understanding of the precise origins and pathophysiology of neonatal encephalopathy and cerebral palsy can logical hypotheses be designed and tested to reduce their occurrence. As such, we recommend several important areas of research that are detailed in the text of the full document. We encourage those engaged in research to pursue these areas, and others to exert influence to the degree possible to propel this to a high priority for funding and study.

Finally, we acknowledge our many consultants and support staff who made this project possible. Additionally, the input from and endorsement by the Centers for Disease Control and Prevention, U.S. Department of Health and Human Services; March of Dimes Birth Defects Foundation; National Institute of Child Health and Human Development, National Institutes of Health, U.S. Department of Health and Human Services; the Royal Australian and New Zealand College of Obstetricians and Gynaecologists; the Society for Maternal- Fetal Medicine; and the Society of Obstetricians and Gynaecologists of Canada has resulted in one of the most highly peer-reviewed and scientifically rigorous documents ever published on this topic.

To purchase additional copies of the complete report, contact the ACOG Distribution Center at 800-762-2264 ext. 277 and ask for item # AA432, or order online at sales.acog.org. Follow the path from the ACOG Bookstore to Professional Publications to ACOG Guidelines.