Hypothermia as a Treatment for Birth Asphyxia

Shankaran, Seetha; Laptook, Abbot R.

doi:10.1097/grf.0b013e31811eba5e

Cited by 35 publications

(24 citation statements)

References 53 publications

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“…The combined findings stress the importance of comparing and contrasting HI injury in both preterm and term infants relative to follow-up morbidity, plasticity and long-term behavioral development. They also heighten the urgency to continue a search for neuroprotective interventions such as whole body/head cooling or erythropoietin in term HIE infants [91–92]. Finally, our findings also show subtle but significant early RAP deficits and robust attention deficits in a preterm HI model, emphasizing the importance of developing new interventions for this population as well.…”

Section: 5 Conclusionsupporting

confidence: 59%

Behavioral and histological outcomes following neonatal HI injury in a preterm (P3) and term (P7) rodent model

Alexander

Garbus

Smith

et al. 2014

Behavioural Brain Research

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Hypoxia-ischemia (HI) occurs when blood and/or oxygen delivery to the brain is compromised. HI injuries can occur in infants born prematurely (<37 weeks gestational age) or at very low birth weight (<1500 grams), as well as in term infants with birth complications. In both preterm and term HI populations, brain injury is associated with subsequent behavioral deficits. Neonatal HI injury can be modeled in rodents (e.g., the Rice-Vannucci method, via cautery of right carotid followed by hypoxia). When this injury is induced early in life (between postnatal day (P)1–5), neuropathologies typical of human preterm HI are modeled. When injury is induced later (P7–12), neuropathologies typical of those seen in HI term infants are modeled. The current study sought to characterize the similarities/differences between outcomes following early (P3) and late (P7) HI injury in rats. Male rats with HI injury on P3 or P7, as well as sham controls, were tested on a variety of behavioral tasks in both juvenile and adult periods. Results showed that P7 HI rats displayed deficits on motor learning, rapid auditory processing (RAP), and other learning/memory tasks, as well as a reduction in volume in various neuroanatomical structures. P3 HI animals showed only transient deficits on RAP tasks in the juvenile period (but not in adulthood), yet robust deficits on a visual attention task in adulthood. P3 HI animals did not show any significant reductions in brain volume that we could detect. These data suggest that: 1) behavioral deficits following neonatal HI are task-specific depending on timing of injury; 2) P3 HI rats showed transient deficits on RAP tasks; 3) the more pervasive behavioral deficits seen following P7 HI injury were associated with substantial global tissue loss; and 4) persistent deficits in attention in P3 HI subjects might be linked to neural connectivity disturbances rather than a global loss of brain volume, given that no such pathology was found. These combined findings can be applied to our understanding of differing long-term outcomes following neonatal HI injury in premature versus term infants.

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Section: 5 Conclusionsupporting

confidence: 59%

Behavioral and histological outcomes following neonatal HI injury in a preterm (P3) and term (P7) rodent model

Alexander

Garbus

Smith

et al. 2014

Behavioural Brain Research

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“…While a number of different agents have shown a neuroprotective effect in animal models of HI, hypothermia is the only therapeutic intervention that has been extensively investigated in the newborn patient population 8, 150-153. This clinical investigation was preceded by a large number of preclinical studies in multiple animal models that demonstrated a neuroprotective effect 90, 154-159.…”

Section: Mechanisms Of Hypothermic Protection In Hypoxia-ischemiamentioning

confidence: 99%

Hypoxic-Ischemic Encephalopathy in the Term Infant

Fatemi

Wilson

Johnston

2009

Clinics in Perinatology

226

174

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SynopsisHypoxia-ischemia in the perinatal period is an important cause of cerebral palsy and associated disabilities in children. There has been significant research progress in hypoxic-ischemic encephalopathy over the last two decades and many new molecular mechanisms have been identified. Despite all these advances, therapeutic interventions are still limited. In this review paper, we discuss a number of molecular pathways involved in hypoxia-ischemia, and potential therapeutic targets. KeywordsHypoxia ischemia; neonatal encephalopathy; apoptosis; oxidative stress; hypothermia IntroductionHypoxia-ischemia in the perinatal period is an important cause of cerebral palsy and associated disabilities in children. Cerebral palsy is one of the most costly neurologic disabilities because of its frequency (2/1000 births) and persistence over the life span. 1 In the term infant, the most common mechanism of hypoxic injury is intrauterine asphyxia brought on by circulatory problems, such as clotting of placental arteries, placental abruption, or inflammatory processes. 2 These result in perinatal depression leading to diminished exchange of oxygen and carbon dioxide and severe lactic acidosis. 2 A recent study by Graham et al showed that the incidence of neonatal neurologic morbidity and mortality for term infants born with cord pH < 7.0 is approximately 25%. 3 Reduced cardiac output in the setting of hypoxia is referred to as hypoxiaischemia (HI). 4 If an episode of HI is severe enough to damage the brain, it leads within 12 to 36 hours to a neonatal encephalopathy known as hypoxic-ischemic encephalopathy (HIE). 5 This clinical syndrome includes seizures, epileptic activity on electroencephalogram (EEG), Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access Author ManuscriptClin Perinatol. Author manuscript; available in PMC 2010 December 1. Published in final edited form as:Clin Perinatol. 2009 December ; 36(4): 835-vii. doi:10.1016/j.clp.2009.011. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript hypotonia, poor feeding, and a depressed level of consciousness that typically lasts from 7-14 days. 6 Pathology studies of term neonates who sustained a profound hypoxic-ischemic event show relative cortical sparing and deep gray matter injury particularly involving hippocampi, lateral geniculate nuclei, putamen, ventrolateral thalami, and dorsal mesencephalon. 7 There is no effective pharmacologic therapy, although hypothermia has shown promise in several clinical trials. 8,9 Magnetic resonance imaging (MRI) has markedly improved the understanding ...

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“…In birth asphyxia, the infant needs immediate professional care in the neonatal intensive care unit (NICU; Long & Brandon, 2007), and hypothermia treatment is a method for treating HIE following birth asphyxia (Shankaran & Laptook, 2007) to reduce the risk of brain injury (Yager, Armstrong, Jaharus, Saucier, & Wirrell, 2004). Hypothermia treatment was introduced in 2005 in several neonatal units in various countries that participated in Total Body Cooling trial (TOBY), an English multi-center study (Azzopardi et al, 2009).…”

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confidence: 99%

Becoming a parent to a child with birth asphyxia—From a traumatic delivery to living with the experience at home

Heringhaus

Dellenmark‐Blom

Wigert

2013

International Journal of Qualitative Studies on Health and Well

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The aim of this study is to describe the experiences of becoming a parent to a child with birth asphyxia treated with hypothermia in the neonatal intensive care unit (NICU). In line with the medical advances, the survival of critically ill infants with increased risk of morbidity is increasing. Children who survive birth asphyxia are at a higher risk of functional impairments, cerebral palsy (CP), or impaired vision and hearing. Since 2006, hypothermia treatment following birth asphyxia is used in many of the Swedish neonatal units to reduce the risk of brain injury. To date, research on the experience of parenthood of the child with birth asphyxia is sparse. To improve today's neonatal care delivery, health-care providers need to better understand the experiences of becoming a parent to a child with birth asphyxia. A total of 26 parents of 16 children with birth asphyxia treated with hypothermia in a Swedish NICU were interviewed. The transcribed interview texts were analysed according to a qualitative latent content analysis. We found that the experience of becoming a parent to a child with birth asphyxia treated with hypothermia at the NICU was a strenuous journey of overriding an emotional rollercoaster, that is, from being thrown into a chaotic situation which started with a traumatic delivery to later processing the difficult situation of believing the child might not survive or was to be seriously affected by the asphyxia. The prolonged parent–infant separation due to the hypothermia treatment and parents’ fear of touching the infant because of the high-tech equipment seemed to hamper the parent–infant bonding. The adaption of the everyday life at home seemed to be facilitated by the follow-up information of the doctor after discharge. The results of this study underline the importance of family-centered support during and also after the NICU discharge.

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Hypothermia as a Treatment for Birth Asphyxia

Cited by 35 publications

References 53 publications

Behavioral and histological outcomes following neonatal HI injury in a preterm (P3) and term (P7) rodent model

Behavioral and histological outcomes following neonatal HI injury in a preterm (P3) and term (P7) rodent model

Hypoxic-Ischemic Encephalopathy in the Term Infant

Becoming a parent to a child with birth asphyxia—From a traumatic delivery to living with the experience at home

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