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Preterm EEG: A Multimodal Neurophysiological Protocol
Published on: February 18, 2012
The ABCs of electronic fetal monitoring
1Department of Obstetrics, Gynecology, AMI Encino-Tarzana Regional Medical Center, Calif.
There have been too many surrogates used to define fetal asphyxia and too many surrogates used to time fetal injury. Low Apgar scores and the need for prolonged resuscitation, by themselves, are inadequate criteria for the diagnosis of perinatal asphyxia or subsequent neurologic handicap. Even with the addition of a low cord pH and seizures, it is not possible to infer neurologic handicap. Furthermore, acidosis and depression at birth (which should be referred to as "perinatal asphyxia") cannot measure the duration and extent of any prenatal asphyxial encounter. Nor can we use the absence of one or more of these signs to exclude perinatal asphyxia as the cause of injury. We cannot refer to fetal asphyxia and injury therefrom without defining our criteria and describing the model of asphyxia being invoked. Because ischemia to the brain and other organs (that is, localized asphyxia), not systemic global asphyxia, appears to be the major precursor of human fetal injury it seems unreasonable to insist on systemic fetal asphyxia at any time to validate the timing or mechanism of fetal injury. Most hypoxic newborn infants are not injured and most injured newborn infants are not hypoxic. Furthermore, that a baby is injured as a result of hypoxia during labor does not mean that the hypoxia was preventable. FHR patterns, properly interpreted, may be one of the most reliable determinants of subsequent neurologic outcome and depending on the circumstances may provide insight into the timing and mechanism of neurologic injury.(ABSTRACT TRUNCATED AT 250 WORDS)
There have been too many surrogates used to define fetal asphyxia and too many surrogates used to time fetal injury. Low Apgar scores and the need for prolonged resuscitation, by themselves, are inadequate criteria for the diagnosis of perinatal asphyxia or subsequent neurologic handicap. Even with the addition of a low cord pH and seizures, it is not possible to infer neurologic handicap. Furthermore, acidosis and depression at birth (which should be referred to as "perinatal asphyxia") cannot measure the duration and extent of any prenatal asphyxial encounter. Nor can we use the absence of one or more of these signs to exclude perinatal asphyxia as the cause of injury. We cannot refer to fetal asphyxia and injury therefrom without defining our criteria and describing the model of asphyxia being invoked. Because ischemia to the brain and other organs (that is, localized asphyxia), not systemic global asphyxia, appears to be the major precursor of human fetal injury it seems unreasonable to insist on systemic fetal asphyxia at any time to validate the timing or mechanism of fetal injury. Most hypoxic newborn infants are not injured and most injured newborn infants are not hypoxic. Furthermore, that a baby is injured as a result of hypoxia during labor does not mean that the hypoxia was preventable. FHR patterns, properly interpreted, may be one of the most reliable determinants of subsequent neurologic outcome and depending on the circumstances may provide insight into the timing and mechanism of neurologic injury.(ABSTRACT TRUNCATED AT 250 WORDS)
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