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Neonatal encephalopathy is an important clinical condition with which all providers of newborn care should be familiar. It is a condition that is defined and characterized by the findings on physical examination and includes combinations of abnormalities in level of consciousness, muscle tone, activity, reflexes, brainstem function/breathing patterns, seizures, and ability to feed. In the past, these findings have been equated with hypoxia-ischemia or asphyxia as an etiology; however, more comprehensive assessments of neonatal encephalopathy indicated that a casual relationship between encephalopathy and hypoxia-ischemia is not as common as previously thought. What has emerged is the concept that neonatal encephalopathy is a phenotype for a broad array of potential diagnoses in the neonatal period and is without any preconceived implications regarding the timing of events that precipitate neonatal encephalopathy. The term neonatal rather than newborn encephalopathy is more appropriate because this is a condition that may be present at birth or develop at some time after birth. Thus, the objectives of this chapter are to provide an overview of

  1. Epidemiology of neonatal encephalopathy

  2. Outcome of infants with neonatal encephalopathy

  3. Spectrum of diagnoses that may be associated with neonatal encephalopathy


Meaningful information regarding the incidence of neonatal encephalopathy can only be derived from population-based studies. This type of study avoids referral bias because hospital-based (even tertiary hospitals) studies represent referral centers. Other methodological considerations include case ascertainment (retrospective reviews without clear definitions vs prospective data collection with a priori definitions) and use of the appropriate denominator of infants at risk for neonatal encephalopathy.1 Estimates of the incidence of neonatal encephalopathy prior to the mid-1990s have been limited to small studies that were not population based and focused on intrapartum events to determine the presence or absence of hypoxia-ischemia. Since that time, there have been 3 population-based studies to examine the epidemiology of neonatal encephalopathy, but all represent work from more than 10 years ago.

A population-based, unmatched, case-control study was performed between 1993 and 1995 of infants with encephalopathy born in Western Australia around the metropolitan area of Perth.2 All cases of moderate or severe encephalopathy were referred to 1 of 2 tertiary neonatal intensive care units. This investigation focused on term infants in the first week of life using predetermined inclusion criteria of encephalopathy. Inclusion criteria were purposefully broad and included any 2 of specific variables, which needed to last more than 24 hours (abnormal consciousness, difficulty maintaining respirations of a presumed central origin, difficulty feeding, or abnormal tone and reflexes) or seizures alone. Deaths in the first week of life were reviewed to avoid exclusion of infants dying prior to transfer with evidence of encephalopathy. During the study interval, 164 cases of neonatal encephalopathy were identified. The incidence of neonatal encephalopathy was 3.8 per 1000 live term births (95% confidence interval, 3.2–4.4).

During the same years, 1993–1995, ...

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