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Management and investigation of neonatal encephalopathy: 2017 update
  1. Kathryn Martinello1,
  2. Anthony R Hart2,
  3. Sufin Yap3,
  4. Subhabrata Mitra1,
  5. Nicola J Robertson1
  1. 1Department of Neonatology, Institute for Women's Health, University College London, UK
  2. 2Department of Neonatal and Paediatric Neurology, Sheffield Children's Hospital NHS Foundation Trust, Sheffield, UK
  3. 3Department of Inherited Metabolic Diseases, Sheffield Children's Hospital NHS Foundation Trust, Sheffield, UK
  1. Correspondence to Professor Nicola J Robertson, Institute for Women's Health, University College London, 74 Huntley Street, London WC1E 6AU, UK; n.robertson{at}ucl.ac.uk

Abstract

This review discusses an approach to determining the cause of neonatal encephalopathy, as well as current evidence on resuscitation and subsequent management of hypoxic-ischaemic encephalopathy (HIE). Encephalopathy in neonates can be due to varied aetiologies in addition to hypoxic-ischaemia. A combination of careful history, examination and the judicious use of investigations can help determine the cause. Over the last 7 years, infants with moderate to severe HIE have benefited from the introduction of routine therapeutic hypothermia; the number needed to treat for an additional beneficial outcome is 7 (95% CI 5 to 10). More recent research has focused on optimal resuscitation practices for babies with cardiorespiratory depression, such as delayed cord clamping after establishment of ventilation and resuscitation in air. Around a quarter of infants with asystole at 10 min after birth who are subsequently cooled have normal outcomes, suggesting that individualised decision making on stopping resuscitation is needed, based on access to intensive treatment unit and early cooling. The full benefit of cooling appears to have been exploited in our current treatment protocols of 72 hours at 33.5°C; deeper and longer cooling showed adverse outcome. The challenge over the next 5–10 years will be to assess which adjunct therapies are safe and optimise hypothermic brain protection in phase I and phase II trials. Optimal care may require tailoring treatments according to gender, genetic risk, injury severity and inflammatory status.

  • neonatal encephalopathy
  • hypoxic ischaemic encephalopathy
  • neuroprotection
  • resuscitation of the newborn

This is an Open Access article distributed in accordance with the terms of the Creative Commons Attribution (CC BY 4.0) license, which permits others to distribute, remix, adapt and build upon this work, for commercial use, provided the original work is properly cited. See: http://creativecommons.org/licenses/by/4.0/

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Footnotes

  • Contributors KM and ARH wrote the first draft. SM wrote the section on NIRS and revised and commented on the manuscript. NJR revised and updated the whole manuscript, ARH and SY revised and updated sections on NE investigation.

  • Funding  This project was supported by the National Institute for Health Research University College London Hospitals Biomedical Research Centre. This study was funded by MRC grant MR/M006743/1.

  • Competing interests NJR has received a research grant from Chiesi Pharmaceuticals and from Air Liquid for preclinical work on melatonin and argon, respectively.

  • Provenance and peer review Commissioned; externally peer reviewed.

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