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Neonatal encephalopathy

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Neonatal encephalopathy
Other namesHypoxic and ischemic brain injury in the newborn, perinatal asphyxia, neonatal hypoxic and ischemic brain injury
SpecialtyPediatrics Edit this on Wikidata

Neonatal encephalopathy (NE), also known as neonatal hypoxic-ischemic encephalopathy (neonatal HIE or NHIE), is defined by signs and symptoms of abnormal neurological function in the first few days of life in an infant born at term.[1] In this condition there is difficulty initiating and maintaining respirations, a subnormal level of consciousness, and associated depression of tone, reflexes, and possibly seizures.[2] Encephalopathy is a nonspecific response of the brain to injury which may occur via multiple methods, but is commonly caused by birth asphyxia, leading to cerebral hypoxia.[1][2]

Signs and symptoms

In neonates born at or beyond 35 weeks, neonatal encephalopathy may present itself as the following symptoms:[citation needed]

  • Reduced level of consciousness
  • Seizures (which peak at 48 hours)
  • Difficulty initiating and maintaining respiration
  • Depression of tone and reflexes[3]

Diagnosis

Cord blood gas analysis can be used to determine if there is perinatal hypoxia/asphyxia, which are potential causes of hypoxic-ischemic encephalopathy or cerebral palsy, and give insight into causes of intrapartum fetal distress.[4] Cord blood gas analysis is indicated for high-risk pregnancies, in cases where C-sections occurred due to fetal compromise, if there were abnormal fetal heart rate patterns, Apgar scores of 3 or lower, intrapartum fever, or multifetal gestation.[citation needed]

Evidence of brain injury related to the hypoxic-ischemic events that cause neonatal encephalopathy can be seen with brain MRIs, CTs, magnetic resonance spectroscopy imaging or ultrasounds.[5][6]

Neonatal encephalopathy may be assessed using Sarnat staging.[citation needed]

Treatment

Main article: Hypothermia therapy for neonatal encephalopathy

In the past, treatment options were limited to supportive medical therapy.[7] Currently, neonatal encephalopathy is treated using hypothermia therapy.[8] This has been shown to reduce brain damage, reduce future disability, and improve survival.[9] Hypothermia therapy is also sometimes termed hypothermic neural rescue therapy. Clinical trials are taking place to investigate the effectiveness of stem cell-based interventions, which are thought to have the potential to reduce mortality and improve the long-term development of newborn infants with neonatal encephalopathy.[10]

Prognosis

HIE is a major predictor of neurodevelopmental disability in term infants. 25 percent have permanent neurological deficits.[11]

It can result in developmental delay or periventricular leukomalacia.[citation needed]

Epidemiology

Overall, the relative incidence of neonatal encephalopathy is estimated to be between 2 and 9 per 1000 term births.[3] 40% to 60% of affected infants die by 2 years old or have severe disabilities.[7] In 2013 it was estimated to have resulted in 644,000 deaths down from 874,000 deaths in 1990.[12]

References

  1. ^ a b "Neonatal Encephalopathy". adhb.govt.nz. Retrieved 7 March 2015.
  2. ^ a b Neurology. Perlman, Jeffrey M., Polin, Richard A. (Richard Alan), 1945-. Philadelphia: Saunders/Elsevier. 2008. ISBN 9781416031574. OCLC 489075193.{{cite book}}: CS1 maint: others (link)
  3. ^ a b "Clinical features, diagnosis, and treatment of neonatal encephalopathy". www.uptodate.com. Retrieved 2016-03-24.
  4. ^ Armstrong, L; Stenson, BJ (November 2007). "Use of umbilical cord blood gas analysis in the assessment of the newborn". Archives of Disease in Childhood: Fetal and Neonatal Edition. 92 (6): F430–4. doi:10.1136/adc.2006.099846. PMC 2675384. PMID 17951550.
  5. ^ Pediatrics, American Academy of (2014-05-01). "Neonatal Encephalopathy and Neurologic Outcome, Second EditionReport of the American College of Obstetricians and Gynecologists' Task Force on Neonatal Encephalopathy". Pediatrics. 133 (5): e1482–e1488. doi:10.1542/peds.2014-0724. ISSN 0031-4005.
  6. ^ "Identifying HIE: Diagnostic Tests and Medical Evaluations". HIE Help Center. Retrieved 2017-11-16.
  7. ^ a b Allen, Kimberly A.; Brandon, Debra H. (2011-09-01). "Hypoxic Ischemic Encephalopathy: Pathophysiology and Experimental Treatments". Newborn and Infant Nursing Reviews. Neuroprotective Strategies. 11 (3): 125–133. doi:10.1053/j.nainr.2011.07.004. PMC 3171747. PMID 21927583.
  8. ^ Services, c=AU; st=Victoria; o=State Government of Victoria; ou1=Department of Health and Human. "Encephalopathy in neonates: Neonatal ehandbook - Department of Health and Human Services, Victoria, Australia". www.health.vic.gov.au. Retrieved 2016-03-24.{{cite web}}: CS1 maint: multiple names: authors list (link) CS1 maint: numeric names: authors list (link)
  9. ^ Jacobs, Susan E.; Berg, Marie; Hunt, Rod; Tarnow-Mordi, William O.; Inder, Terrie E.; Davis, Peter G. (2013-01-31). "Cooling for newborns with hypoxic ischaemic encephalopathy". The Cochrane Database of Systematic Reviews (1): CD003311. doi:10.1002/14651858.CD003311.pub3. ISSN 1469-493X. PMC 7003568. PMID 23440789.
  10. ^ Bruschettini, M; Romantsik, O; Moreira, A; Ley, D; Thébaud, B (19 August 2020). "Stem cell-based interventions for the prevention of morbidity and mortality following hypoxic-ischaemic encephalopathy in newborn infants". The Cochrane Database of Systematic Reviews. 8: CD013202. doi:10.1002/14651858.CD013202.pub2. PMC 7438027. PMID 32813884.
  11. ^ Graham, Ernest M.; Ruis, Kristy A.; Hartman, Adam L.; Northington, Frances J.; Fox, Harold E. (December 2008). "A systematic review of the role of intrapartum hypoxia-ischemia in the causation of neonatal encephalopathy". American Journal of Obstetrics and Gynecology. 199 (6): 587–595. doi:10.1016/j.ajog.2008.06.094. PMID 19084096.
  12. ^ GBD 2013 Mortality and Causes of Death, Collaborators (17 December 2014). "Global, regional, and national age-sex specific all-cause and cause-specific mortality for 240 causes of death, 1990-2013: a systematic analysis for the Global Burden of Disease Study 2013". Lancet. 385 (9963): 117–71. doi:10.1016/S0140-6736(14)61682-2. PMC 4340604. PMID 25530442. {{cite journal}}: |first1= has generic name (help)CS1 maint: numeric names: authors list (link)
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