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Fetal and Neonatal Encephalopathy
Response to Dr Elliott by Dr Savman
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Stephen J Elliott, MD UCSF-Fresno
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selliott{at}communitymedical.org Stephen J Elliott
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Dr. Savman has provided a thoughtful review of neonatal brain dysfunction. Several points deserve consideration. The term "birth asphyxia" is strongly discouraged in many circles because of the (erroneous) implication of a cause and effect, namely that the birth process linearly causes asphyxia. Indeed, many encephalopathic newborns may have been encephalopathic for an extended period of time prior to the onset of labor. For this reason, we teach and promote the term "Neonatal Encephalopathy" (although a case might be made for "Fetal Encephalopathy" or "Fetoneonatal Encephalopathy" if there is evidence for such). The review closely links the terms "birth asphyxia" and "hypoxic- ischemic encephalopathy". It is important to note, however, that other pathophysiologies, besides hypoxia-ischemia, result in neonatal encephalopathy. These include brain malformations, drugs, infections and metabolic disease. When considering infants delivered with low Apgar scores, we teach our students not to assume or jump to an assertion of hypoxic-ischemic encephalopathy until other etiologies for the encephalopathy have been ruled out. Finally, the review states "Because neonatal encephalopathy is multifactorial, it must be preceded by signs of intrapartum asphyxia,...". Most obstetricians and neonatologists have been surprised at one time or another by an infant who has a fully unremarkable intrapartum course and yet who is encephalopathic ("depressed") at delivery. In these cases, the encephalopathy probably predated intrapartum events. Conflict of Interest:None declared |
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Karin Savman, neonatologist Gottenberg University,Sweden
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karin.savman{at}pediat.gu.se Karin Savman
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" I am grateful for the valuable and clarifying comments made by Dr Elliott. I fully agree that neonatal encephalopathy is in many (or most) cases caused by other factors than intrapartum asphyxia, that there are multiple infants with neonatal encephalopathy that have no signs of intrapartal distress, that low APGAR score is not a good indicator for asphyxia and that there is no linear relation between hypoxia-ischemia and encephalopathy. There is, however, strong experimental and clinical evidence that intrapartum asphyxia (defined as impaired oxygen and energy delivery during delivery) can indeed cause encephalopathy as well as permanent and often severe hypoxic-ischemic brain injury. The review focuses on this limited, but clinically important, group of infants and the mechanisms of injury within this group. The new prospects of neuroprotective treatments such as hypothermia makes it even more important to identify, among other encephalopathic infants, those who indeed suffer from intrapartum asphyxia and where secondary brain injury mechanisms may be of importance. As pointed out in the review, this requires strict criteria for intrapartum inadequate oxygen delivery, most importantly a significant metabolic acidosis. Such criteria are applied to identify infants where hypoxia-ischemia is a probable cause of neonatal enchephalopathy and that may benefit from neuroprotective treatment. As stated in the review, this does not exclude infants with contributing factors other than asphyxia, but will hopefully narrow the group and help us with a more stringent definition of encephalopathy and its causes. I think that Dr Elliott and I fully agree on the need for such definitions, as well as the need to identify infants at risk of developing hypoxic-ischemic injury, although we approached the subject from somewhat different angles." Conflict of Interest:None declared |
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