Original ArticlesThe Syndrome of Acute Near-Total Intrauterine Asphyxia in the Term Infant
Introduction
Infant laboratory animals subjected to hypoxic-ischemic insult demonstrate two distinct patterns of damage [1]. Prolonged partial asphyxia damages cerebral cortex and cerebral white matter, beginning in parasagittal (watershed) regions. In contrast, brief total asphyxia damages subcortical nuclei in the thalamus and brainstem and, if preceded by subthreshold partial asphyxia, basal ganglia. Imaging studies in infants have documented two similar patterns of abnormality. Early reports suggested that intrauterine asphyxia in term infants preferentially damaged the cerebral cortex and underlying white matter [2]. More recently, widespread use of magnetic resonance imaging (MRI) has revealed a subgroup of infants in whom damage occurs predominantly in subcortical gray structures, especially basal ganglia and thalamus. The clinical syndromes corresponding to these two patterns of damage have not yet been defined fully. Most previous reports of subcortical damage have emphasized imaging abnormalities and included only limited clinical description 3, 4, 5, 6, 7. In the few case reports with detailed clinical descriptions 8, 9, 10, 11 the responsible insult appeared to be a sudden, severe asphyxia with relatively brief but profound cardiocirculatory and respiratory compromise near the time of delivery, similar to the paradigm of acute total asphyxia with preceding partial asphyxia in experimental animals. Therefore, we reviewed our experience with infants who were likely to have suffered an acute near-total hypoxic-ischemic insult to better define the spectrum of their clinical and radiologic features.
Section snippets
Patients and Methods
We sought to identify as homogeneous a group as possible of infants who had sustained an acute, near-total intrauterine hypoxic-ischemic insult that was of sufficient severity to damage the brain. Therefore, we limited our consideration to infants who had experienced neonatal seizures as detected by typical clinical criteria [12] because seizures are an indication of a significant encephalopathy and a relatively good predictor of neurologic sequelae [13]. Eighty-five infants hospitalized in the
Features During Labor
In nine patients, electronic fetal monitoring was performed as a routine method of assessing fetal well-being during labor and was felt to be reassuring until the onset of the persistent terminal bradycardia (Table 1). In one patient (case 4) a few moderate variable decelerations were noted 3 hours before delivery; the decelerations resolved spontaneously, and no further decelerations were noted before the bradycardia. In another patient (case 3), two moderate variable decelerations were noted
Discussion
The goal of this study was to better define the spectrum of neurologic abnormalities in term infants who sustained brain injury from an acute near-total intrauterine hypoxic-ischemic insult. We selected our patients based on criteria that involved results of fetal monitoring and neonatal condition. For inclusion, patients had to have experienced a prolonged persistent bradycardia at the end of labor that did not recover before delivery and neonatal seizures. In 9 of our 11 patients, fetal
Acknowledgements
The authors thank the staff of the Division of Neonatology, Evanston Hospital, for monitoring data on cases 4 and 10. We also thank Barbara L. Trommer, MD, for follow-up data on case 5, for helpful review of the manuscript, and for many helpful discussions during the preparation of this report.
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