Clinics in perinatology
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The basic mechanism of kernicterus and bilirubin encephalopathy has not been unequivocally determined. Much knowledge has been gained about phenomena that contribute to bilirubin neurotoxicity, and this knowledge has implications for clinical practice. Conditions that impact on blood-brain barrier function, increase brain blood flow, or impact on bilirubin metabolism, including its transport in serum, should be avoided, if possible. ⋯ If these conditions are not avoidable then there should be a more aggressive approach to the treatment of hyperbilirubinemia. The limits of tolerance for hyperbilirubinemia varies among neonates and there are no tools to determine with certainty when a particular infant is approaching the danger zone. Neurological symptoms in a jaundiced infant require extreme vigilance, and, in most cases, immediate intervention.
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Clinics in perinatology · Dec 2002
ReviewAdvances in postnatal neuroimaging: relevance to pathogenesis and treatment of brain injury.
The human brain is susceptible to a wide variety of insults. The permanent residua of these abnormalities are represented in dysfunction of one or more areas of neurodevelopment. ⋯ Advanced magnetic resonance techniques, such as quantitative morphometric magnetic resonance techniques, diffusion-weighted magnetic resonance techniques, and magnetic resonance spectroscopy applied to the study of early human brain development have given us a better understanding of the pathophysiologic mechanisms of brain injury and its effects on subsequent brain development. Magnetic resonance imaging has provided an invaluable tool for the study of the fetal and newborn brain in vivo.
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Clinics in perinatology · Dec 2002
ReviewThe effects of temperature on hypoxic-ischemic brain injury.
Over the past 15 years it has been recognized that the temperature of the brain has an important influence on the extent of brain injury that follows intervals of hypoxia-ischemia. Available data in animals and humans show that brain injury is worsened when fever is superimposed on an ischemic event. Furthermore, data in neonates and adults strongly suggest a neuroprotective role for modest hypothermia (temperature reductions of 1 to 6 degrees C) applied during or following ischemia or hypoxia-ischemia. This article provides an overview of the effects of brain temperature, including its role in the development of brain injury, mechanisms of brain injury which may be temperature sensitive, the regulation of brain temperature, thermal characteristics during brain cooling, and current clinical investigations that use temperature as a therapeutic modality.
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Investigations in animal models of hypoxic-ischemic injury have not translated into clinical trials of success because of the complex pathology of hypoxic-ischemic brain injury in neonates, the difficulty in defining the onset and duration and severity of the injury, the underlying predisposing disorders of the mothers or the infant, the side effects of many of the investigational drugs precluded clinical use, and many of the investigational agents interfered with only one step of the cascade of events that lead to brain injury. It is possible that a combination of therapeutic agents, including those that affect different levels of the cascade to cell death, will have the greatest neuroprotective effects. Modest hypothermia postpones secondary energy failure and can prolong the window while pharmacotherapeutic agents can be used. It is possible that in the future, sequential administration of agents or strategies that are initiated in the intrapartum period and continued postnatally will be the optimum method for treating infants who are at highest risk for brain injury following acute hypoxic-ischemic asphyxia.