Summary of the Publication, "Neonatal Encephalopathy and Cerebral Palsy: Defining the Pathogenesis and Pathophysiology," by the ACOG Task Force on Neonatal Encephalopathy and Cerebral Palsy

Peter Van Eerden, MD; Peter S. Bernstein, MD, MPH

Disclosures

July 03, 2003

In This Article

Introduction

In January 2003, the American College of Obstetricians and Gynecologists (ACOG) and the American Academy of Pediatrics (AAP) released a publication entitled Neonatal Encephalopathy and Cerebral Palsy: Defining the Pathogenesis and Pathophysiology.[1] The Task Force met over a period of 3 years and worked with expert consultants, conducted a literature review, and received input and endorsements from professional societies and organizations. It is the most extensive peer-reviewed document on this subject published to date. The crux of this report is that the majority of newborn brain injury does not occur during labor and delivery. Instead, most instances of neonatal encephalopathy and cerebral palsy are attributed to events that occur prior to the onset of labor.

The report is important for a number of reasons. First, it lists criteria to define whether neonatal encephalopathy and cerebral palsy are the result of actions during labor, and it facilitates the understanding of the causes of neonatal encephalopathy and cerebral palsy. Second, it will hopefully help to reduce future occurrences of these disorders. Finally, it serves as an invaluable resource to healthcare professionals and the legal system for a better understanding of the events leading to neonatal encephalopathy and cerebral palsy, especially in the face of a bad outcome. This document is important, because failure to adequately educate all of those parties involved in such cases has resulted in substantial financial and emotional cost.

The endorsements and support that this report has received come from 6 major federal agencies and professional organizations. They are the Centers for Disease Control and Prevention, the Child Neurology Society, the March of Dimes Birth Defects Foundation, the National Institute of Child Health and Human Development, 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. This article will serve to review and summarize the findings of this important publication.

Briefly, neonatal encephalopathy is defined clinically on the basis of a constellation of findings, including a combination of abnormal consciousness, tone and reflexes, feeding, respirations, or seizures, which can result from many conditions. It may or may not result in permanent neurologic impairment and is not necessarily caused by intrapartum asphyxia. However, the pathway from intrapartum hypoxic-ischemic injury to subsequent cerebral palsy must progress through neonatal encephalopathy. Hypoxic-ischemic encephalopathy (HIE) is defined as neonatal encephalopathy with intrapartum hypoxia in the absence of any other abnormality.

Cerebral palsy is a chronic disability of central nervous system origin characterized by aberrant control of movement and posture, which appears in early life and is not a result of progressive neurologic disease. Spastic diplegia is the only type of cerebral palsy associated with an acute interruption of blood flow.

The historical factors used to define perinatal asphyxia (ie, meconium, Apgar scores) are not specific to the disease process leading to the neurologic damage. Using these nonspecific markers incorrectly identifies individuals as being exposed to "perinatal asphyxia."

The criteria to define an acute intrapartum event sufficient to cause cerebral palsy are listed in the report as follows:

Essential criteria (must meet all 4):

  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 weeks gestation

  3. Cerebral palsy of the spastic quadriplegia 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

These criteria are described in detail at the end of the Task Force's report.

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