Treatment of hypoxic-ischemic encephalopathy in newborns

被引:56
作者
Glass H.C. [1 ]
Ferriero D.M. [1 ]
机构
[1] University of California San Francisco, Neonatal Brain Disorders Center, San Francisco, CA 94143
关键词
Term Infant; Neurodevelopmental Outcome; Perinatal Asphyxia; Fosphenytoin; Neonatal Seizure;
D O I
10.1007/s11940-007-0043-0
中图分类号
学科分类号
摘要
Hypoxic-ishemic (HI) brain injury is the most common cause of encephalopathy and seizures in term newborn infants. There is no single, valid test for birth asphyxia leading to HI brain injury, and thus this disorder is often poorly characterized, and the timing and etiology of the injury can be difficult to ascertain. Optimal management of HI brain injury involves prompt resuscitation, careful supportive care including prevention of hyperthermia and hypoglycemia, and treatment of clinical and frequent or prolonged subclinical seizures. Recent evidence suggests that therapeutic hypothermia by selective head or whole-body cooling administered within 6 hours of birth reduces the incidence of death or moderate/severe disability at 12 to 22 months. Hypothermia is a promising new therapy that physicians should consider within the context of a registry or study. Optimal seizure treatment remains controversial because the most widely used drug, phenobarbital, has limited efficacy, and the value of monitoring and treating subclinical seizures is uncertain. There is compelling need for well-designed clinical trials to address treatment of ongoing brain injury in the setting of hypoxia-ischemia and seizures. Emerging evidence from preclinical studies suggests that future therapy for HI brain injury and neonatal encephalopathy will combine novel neuroprotective and anti-seizure agents. Pilot clinical trials'of newer anticonvulsants are ongoing and will provide critical information for care of neonatal seizures. Copyright © 2007 by Current Medicine Group LLC.
引用
收藏
页码:414 / 423
页数:9
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[1]  
Miller S.P., Latal B., Clark H., Et al., Clinical sips predict 30-month neurodevelopmental outcome after neonatal encephalopathy, Am J Obstet Gynecol, 190, pp. 93-99, (2004)
[2]  
Wirrell E.C., Armstrong E.A., Osman L.D., Et al., Prolonged seizures exacerbate pennatal hypoxic-ischemic brain damage, Pediatr Res, 50, pp. 445-454, (2001)
[3]  
Dzhala V., Ben-Ari Y., Khazipov R., Seizures accelerate anoxia-induced neuronal death in the neonatal rat hippocampus, Ann Neurol, 48, pp. 632-640, (2000)
[4]  
Miller S.P., Weiss J., Barnwell A., Et al., Seizure-associated brain injury in term newborns with perinatal asphyxia, Neurology, 58, pp. 542-548, (2002)
[5]  
Pressler R.M., Boylan G.B., Morton M., Et al., Early serial EEG in hypoxic ischaemic encephalopathy, Clin Neurophysiol, 112, pp. 31-37, (2001)
[6]  
Zeinstra E., Fock J.M., Begeer J.H., Et al., The prognostic value of serial EEG recordings following acute neonatal asphyxia in full-term infants, Eur J Paediatr Neurol, 5, pp. 155-160, (2001)
[7]  
de Vries L.S., Toet M.C., Amplitude integrated electroencephalography in the full-term newborn, Clin Perinatol, 33, pp. 619-632, (2006)
[8]  
Barkovich A.J., MR imaging of the neonatal brain, Neuroimaging Clin N Am, 16, (2006)
[9]  
Barkovich A.J., Miller S.P., Bartha A., Et al., MR imaging, MR spectroscopy, and diffusion tensor imaging of sequential studies in neonates with encephalopathy, AJNR Am J Neuroradiol, 27, pp. 533-547, (2006)
[10]  
Roland E.H., Poskitt K., Rodriguez E., Et al., Perinatal hypoxic-ischemic thalamic injury: Clinical features and neuroimaging, Ann Neurol, 44, pp. 161-166, (1998)