Publication:
La encefalopatía hipóxico-isquémica y su tratamiento con hipotermia activa

Research Projects
Organizational Units
Journal Issue
Abstract
La encefalopatía neonatal se define como una afección que sucede en neonatos nacidos con más de 35 semanas de gestación, que cursan con una función neurológica alterada. La encefalopatía hipóxico-isquémica(EHI), es producida bien por una interrupción de la irrigación cerebral o bien por una isquemia en el entorno del parto, que comprometen a las células neuronales produciendo lesiones en el encéfalo. Este episodio hipóxico-isquemico no se ha conseguido relacionar con una causa clara, ya que se desarrolla a raíz de una serie de eventos precipitados y no predecibles, que hacen imposible su anticipación. En cuanto se produce la lesión, el cuerpo del neonato responde activando una cascada inflamatoria y de reparación con el objetivo de recobrar la capacidad funcional. No obstante, cuando finaliza esta primera cascada inflamatoria la disfunción mitocondrial se sigue desarrollando, algo que desembocará, si no se actúa sobre ella, en una segunda cascada lesional. Esta segunda etapa tendrá lugar entre las 6 y 48 horas posteriores al nacimiento, en la que el cuerpo del neonato liberará células y mediadores endógenos que serán los culpables de una nueva lesión neuronal. La hipotermia activa consiste en el enfriamiento del neonato a 33º durante 72 horas, de tal manera que se interviene sobre la segunda cascada inflamatoria lesional y por tanto se minimizan los daños cerebrales en el neonato. La hipotermia se debe de iniciar en cuanto se es sabe de que el neonato ha sufrido una lesión cerebral. Algunos autores hablan de la llamada “Gold hour”, la primera hora de vida, donde es muy importante actuar.
The neonatal encephalopathy is defined as a condition that occurs in neonates born more than 35 weeks of gestation, presenting an altered neurological function. The incidence of perinatal asphyxia in the United States is reported between 1 and 3 per 1000 births and in Spain it ́s around 0.77 per 1,000 births. Hypoxic-ischemic encephalopathy (HIE), is produced either by an interruption of the cerebral irrigation or by an ischemia in the environment of delivery, which involves the neuronal cells producing lesions in the brain. It has not been possible to relate this Hypoxic-ischemic episode to a clear cause, since it develops as a result of a series of hasty and unpredictable events that make its anticipation impossible. As soon as the injury occurs, the neonate ́s body responds by activating an inflammatory and repair with the aim of recovering functional capacity. However, when this first inflammatory cascade ends, it is known that mitochondrial dysfunction continues to develop, something that will lead, if not acted upon it, in a second lesional cascade. This second stage will take place between 6 and 48 hours after birth, in which the child's body will release endogenous cells and mediators that will be responsible for a new neuronal lesion. Active hypothermia consists in cooling the newborn at 33º for 72 hours, acting upon the second cascade inflammatory lesion, minimizing the cerebral damage in the neonate. Hypothermia should start as soon as it is known that the neonate has suffered a brain injury. Same authors call it "The gold hour", the first hour of life, where it is very important to act.
Description
Keywords
Citation
1. Hayashi N. 2009. Management of Pitfalls for the Successful Clinical Use of Hypothermia Treatment. J Neurotrauma;26(3):445–53. 2. Perlman JM. 2006. Intervention strategies for neonatal hypoxic-ischemic cerebral injury. Clin Ther;28(9):1353–65. 3. Selway LD. 2010. State of the Science. Adv Neonatal Care. 60–6. 4. Sharma D. Golden hour of neonatal life: Need of the hour. 2017. Matern Heal Neonatol Perinatol;3:16. 5. Village EG. 2014. Neonatal Encephalopathy and Neurologic Outcome, Second Edition.Pediatrics. 1482–8;133(5). 6. Al Amrani F, Kwan S, Gilbert G, Saint-Martin C, Shevell M,Wintermark P. 2017. Early Imaging and Adverse Neurodevelopmental Outcome in Asphyxiated Newborns Treated With Hypothermia. Pediatr Neurol; 73:20–7 7. Alkholy UM, Abdalmonem N, Zaki A, Ali YF, Mohamed SA, Abdelsalam NI, et al. 2017. Early predictors of brain damage in full-term newborns with hypoxic ischemic encephalopathy. Neuropsychiatr Dis Treat; 13:2133–9. 8. Arnáez J, García-Alix A, Arca G, Valverde E, Caserío S, Moral MT, et al. 2017. Incidencia de la encefalopatía hipóxico-isquémica e implementación de la hipotermia terapéutica por regiones en España. An Pediatría. 9. Azzopardi D, Brocklehurst P, Edwards D, Halliday H, Levene M, Thoresen M, et al.2008. The TOBY Study. Whole body hypothermia for the treatment of perinatal asphyxial encephalopathy: a randomised controlled trial. BMC Pediatric; 8:17. 10. Basu SK, Kaiser JR, Guffey D, Minard CG, Guillet R, Gunn AJ, et al. 2016. Hypoglycaemia and hyperglycaemia are associated with unfavourable outcome in infants with hypoxic ischaemic encephalopathy: a post hoc analysis of the CoolCap Study. Arch Dis Child - Fetal Neonatal Ed; 101(2):F149–55. 11. Chiang M-C, Jong Y-J, Lin C-H. 2017. Therapeutic Hypothermia for Neonates with Hypoxic Ischemic Encephalopathy. Pediatr Neonatol. 12. Flynn JM, Miller F. 2002. Management of hip disorders in patients with cerebral palsy.J Am Acad Orthop Surg.;10(3):198–209. 13. Fredricks TR, Gibson, C, Essien, F, Benseler JS. 2017. Therapeutic Hypothermia to Treat a Newborn With Perinatal Hypoxic-Ischemic Encephalopathy. J Am Osteopath Assoc;117(6):393 14. García-Alix A, Martínez-Biarge M, Diez J, Gayá F, Quero J. 2009. Incidencia y prevalencia de la encefalopatía hipoxico-isquémica en la primera década del siglo xxi. An Pediatría;71(4):319–26. 15. Jacobs SE, Berg M, Hunt R, Tarnow-Mordi WO, Inder TE, Davis PG. 2013. Cooling for newborns with hypoxic ischaemic encephalopathy.Chichester, UK: John Wiley & Sons,Ltd;. p. CD003311. 16. Krägeloh-Mann I, Cans C. 2009. Cerebral palsy update. Brain Dev ;31(7):537-44. 17. Martinello K, Hart AR, Yap S, Mitra S, Robertson NJ.2017. Management and investigationof neonatal encephalopathy: . Arch Dis Child Fetal Neonatal Ed;102(4):F346–58. 18. Rutherford MA, Azzopardi D, Whitelaw A, Cowan F, Renowden S, Edwards AD, et al. 2005. Mild hypothermia and the distribution of cerebral lesions in neonates with hypoxic-ischemic encephalopathy. Pediatrics. ;116(4):1001–6. 19. Wyatt JS, Gluckman PD, Liu PY, Azzopardi D, Ballard R, Edwards AD, et al. 2007.Determinants of outcomes after head cooling for neonatal encephalopathy. Pediatrics.;119(5):912–21.