How Much of Neonatal Encephalopathy Is due to Birth Asphyxia? Karin B.

Nelson, MD, Alan Leviton,

the literature on neonatal encephalopathy, the pervasive assumption is that once infants with major malformations or infections have been excluded, most of the remaining cases are due to birth asphyxia. Assessing the proportion of neonatal encephalopathy that is due to asphyxia during birth is difficult because of problems in defining asphyxia and neonatal encephalopathy and in recognizing the cause of neonatal neurologic illness. Available evidence indicates that neonatal neurologic signs are not strongly related to obstetric complications, signs of fetal distress, or biochemical markers usually considered to indicate perinatal asphyxia. Most studies that have sought positive evidence of independent markers of intrapartum asphyxia have found them to be absent in a large majority of neurologically symptomatic neonates. We conclude that the proportion of neonatal encephalopathy that is asphyxial in origin is not known but warrants examination, especially in view of the probable need in the near future to identify, on the basis of evidence available in the first hour or so of life, suitable candidates for clinical trials of powerful but risky treatments of birth asphyxia. \s=b\ In

(AJDC. 1991;145:1325-1331)

asphyxia Intrapartum versible brain injury in the of lowed

severe

enough

to

produce

irre¬

infant is regularly fol¬ illness in the neonatal

term

by signs neurologic period.13 Neonatal encephalopathy (NE) is a clinically defined syndrome of disturbed neurologic function in the

earliest days of life in the term infant, manifested by dif¬ ficulty with initiating and maintaining respiration, de¬ pression of tone and reflexes, subnormal level of con¬ sciousness, and often by seizures.4 Other names for this syndrome, such as hypoxic-ischemic encephalopathy (HIE) and postasphyxiai encephalopathy, suggest that this syndrome almost always follows recent asphyxia (or hypoxia or ischemia or some combination of these), espe¬ cially during birth. Is it true that NE is usually due to asphyxia? This question gains a fresh urgency because new treatments

Accepted for publication June 3, 1991. From the Neuroepidemiology Branch, National Institute of Neurological Disorders and Stroke, Bethesda, Md (Dr Nelson), and Children's Hospital, and Harvard Medical School, Boston, Mass (Dr Leviton).

Reprint requests

MD 20892 (Dr

to 7550 Wisconsin

Nelson).

Ave, Room 700, Bethesda,

MD

intended to prevent death or long-term neurologic def¬ icits from birth asphyxia are on the horizon.5"10 These powerful and potentially risky therapies will require an ability to identify—and identify very rapidly—infants whose problems are truly secondary to asphyxia at birth and serious enough to warrant some risk in their treatment.

In this article, we review the knowledge base currently available for assessing the fraction of NE that is due to as¬ phyxia at birth and ask how well predictors of neonatal asphyxia that are available within the first hour or two of life permit us to recognize seriously asphyxiated infants who might be candidates for immediate intervention for birth

asphyxia.

DEFINITIONS OF BIRTH ASPHYXIA AND THEIR USE AS PREREQUISITES TO DEFINITIONS OF NE

Asphyxia

major initial problem in assessing the relationship between NE and asphyxia is the lack of generally accepted and operationally defined measures of hypoxia, ischemia, or asphyxia. Asphyxia has been defined as "the depletion of oxygen and the accumulation of carbon dioxide leading to acidosis."11 What level of oxygen depletion, carbon di¬ oxide accumulation, or acidosis warrants the term as¬ A

phyxia?

Defects in oxygénation may be accompanied by hypoperfusion and lead to tissue ischemia. Levels of oxygen or carbon dioxide in the brain are not measured directly. Most investigators of asphyxia in the newborn human have employed instead a variety of the following clinical markers to suggest the presence of asphyxia: meconium in the amniotic fluid, fetal bradycardia, abnormal patterns

of fetal heart rate, abnormalities on blood flow studies or neuroimaging, or biochemical markers. Towell12 has dis¬ cussed the range and variability of these markers. The different approaches of investigators who have impli¬ cated asphyxia and fetal distress adds to the confusion

(Table 1).

NE and In 1976, Sarnat Sarnat2 described 21 depressed newborns with an encephalopathy following fetal dis¬ tress, but they did not provide neurologic criteria for in¬ clusion in the sample. Each infant had an Apgar score less than 6 at 1 or 5 minutes or "a well-defined episode of fetal

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Table 1.—Intranatal

or

Immediate Postnatal

Table

Requirements for Diagnoses

of Newborn Neonatal

Encephalopathy

2.—Similarity of Characteristics Often Taken to Define 'Birth Asphyxia' and 'HIE'* Birth

Characteristics

encephalopathy

Sarnat and Sarnat,21976 One of two criteria Well-defined episode of fetal distress (not defined) Apgar score, «4 at 1 or 5 min

Hypoxie encephalopathy Volpe,271981 Finer et al," 1981 One of three criteria Abnormal heart rate pattern (not defined) Apgar score, «4 at 1 or 5 min Need for immediate resuscitation or intubation Amiel-Tison and Ellison, 1986* One of four criteria Fetal heart rate, 160 beats per min once (?) if by auscultation, prolonged (not defined) if by electronic monitoring Repetitive heart rate decelerations (not defined) Presence of meconium Apgar score,

How much of neonatal encephalopathy is due to birth asphyxia?

In the literature on neonatal encephalopathy, the pervasive assumption is that once infants with major malformations or infections have been excluded,...
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