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• W2000502080 abstract "It is estimated that 4 million American children undergo general anesthesia for a variety of surgical procedures and imaging studies every year. Perioperative mortality and morbidity for children have steadily improved over the last few decades, with a reported mortality rate of one per hundred thousand anesthetics with a tenfold higher rate for young infants.1Flick R.P. Sprung J. Harrison T.E. Perioperative cardiac arrests in children between 1988 and 2005 at a tertiary referral center: A study of 92,881 patients.Anesthesiology. 2007; 106: 226-237Crossref PubMed Scopus (219) Google Scholar More than 20 years ago, it was demonstrated that inadequate anesthesia in young infants undergoing cardiac surgery could lead to an increase in morbidity and mortality due to activation of the surgical stress response.2Anand K.J. Hansen D.D. Hickey P.R. Hormonal-metabolic stress responses in neonates undergoing cardiac surgery.Anesthesiology. 1990; 73: 661-670Crossref PubMed Scopus (307) Google Scholar, 3Anand K.J. Hickey P.R. Halothane-morphine compared with high-dose sufentanil for anesthesia and postoperative analgesia in neonatal cardiac surgery.N Engl J Med. 1992; 326: 1-9Crossref PubMed Scopus (728) Google Scholar, 4Anand K.J. Sippell W.G. Aynsley-Green A. Randomised trial of fentanyl anaesthesia in preterm babies undergoing surgery: Effects on the stress response.Lancet. 1987; 1: 243-248Abstract PubMed Scopus (384) Google Scholar Pediatric anesthesiologists since then have strived to give safe, stress-reducing general anesthetics even to their youngest patients. However, recent animal studies have conclusively shown that most common general anesthetics can induce an increase in neuroapoptosis in juvenile animals. This has led to concerns that general anesthesia administered during the first few years of life may be deleterious for the long-term neurologic development in humans.5Rizzi S. Carter L.B. Ori C. Jevtovic-Todorovic V. Clinical anesthesia causes permanent damage to the fetal guinea pig brain.Brain Pathol. 2008; 18: 198-210Crossref PubMed Scopus (172) Google Scholar, 6Slikker Jr., W. Zou X. Hotchkiss C.E. et al.Ketamine-induced neuronal cell death in the perinatal rhesus monkey.Toxicol Sci. 2007; 98: 145-158Crossref PubMed Scopus (514) Google Scholar, 7Fredriksson A. Ponten E. Gordh T. Eriksson P. Neonatal exposure to a combination of N-methyl-D-aspartate and gamma-aminobutyric acid type A receptor anesthetic agents potentiates apoptotic neurodegeneration and persistent behavioral deficits.Anesthesiology. 2007; 107: 427-436Crossref PubMed Scopus (375) Google Scholar, 8Fredriksson A. Archer T. Alm H. Gordh T. Eriksson P. Neurofunctional deficits and potentiated apoptosis by neonatal NMDA antagonist administration.Behav Brain Res. 2004; 153: 367-376Crossref PubMed Scopus (224) Google Scholar, 9Loepke A.W. Soriano S.G. An assessment of the effects of general anesthetics on developing brain structure and neurocognitive function.Anesth Analg. 2008; 106: 1681-1707Crossref PubMed Scopus (396) Google Scholar, 10Ikonomidou C. Bosch F. Miksa M. et al.Blockade of NMDA receptors and apoptotic neurodegeneration in the developing brain.Science. 1999; 283: 70-74Crossref PubMed Scopus (1750) Google Scholar, 11Jevtovic-Todorovic V. Hartman R.E. Izumi Y. et al.Early exposure to common anesthetic agents causes widespread neurodegeneration in the developing rat brain and persistent learning deficits.J Neurosci. 2003; 23: 876-882Crossref PubMed Google Scholar The implicated anesthetic agents include those that are N-methyl-d-aspartate antagonists (eg, ketamine and nitrous oxide), and gamma amino butyric acid agonists (eg, midazolam, thiopental, propofol, and volatile anesthetics, including sevoflurane): all have been linked with an increase in neuroapoptosis and learning deficits in immature mice, rats, guinea pigs, and rhesus monkeys. The mammalian animal models show an increase in neuroapoptosis only during a specific period during development that corresponds to the animal’s period of rapid brain growth. In addition, general anesthetics have been shown to cause altered dendrite formation, decreased number of glial cells, and decreased neurogenesis in juvenile animals even beyond the period of maximal brain growth.12De Roo M. Klauser P. Briner A. et al.Anesthetics rapidly promote synaptogenesis during a critical period of brain development.PLoS One. 2009; 4: e7043Crossref PubMed Scopus (140) Google Scholar, 13Briner A. De Roo M. Dayer A. Muller D. Habre W. Vutskits L. Volatile anesthetics rapidly increase dendritic spine density in the rat medial prefrontal cortex during synaptogenesis.Anesthesiology. 2010; 112: 546-556Crossref PubMed Scopus (201) Google Scholar, 14Spahr-Schopfer I. Vutskits L. Toni N. Buchs P.A. Parisi L. Muller D. Differential neurotoxic effects of propofol on dissociated cortical cells and organotypic hippocampal cultures.Anesthesiology. 2000; 92: 1408-1417Crossref PubMed Scopus (51) Google Scholar However, there is great difficulty in determining the period of susceptibility to general anesthetic–induced neurotoxicity in humans. The period of maximal brain growth occurs from the last trimester of fetal development to 24 months of age.15Dobbing J. Sands J. Quantitative growth and development of human brain.Arch Dis Child. 1973; 48: 757-767Crossref PubMed Scopus (1182) Google Scholar Although humans have traditionally been considered an altricial species because of their motor immaturity at birth, there is considerable evidence using neuroinformatic techniques that humans may actually be a precocial species and that the period of maximal vulnerability to neurotoxins may occur in utero around the 17th to 22nd week of gestation.16Clancy B. Finlay B.L. Darlington R.B. Anand K.J. Extrapolating brain development from experimental species to humans.Neurotoxicology. 2007; 28: 931-937Crossref PubMed Scopus (661) Google Scholar, 17Clancy B. Kersh B. Hyde J. Darlington R.B. Anand K.J. Finlay B.L. Web-based method for translating neurodevelopment from laboratory species to humans.Neuroinformatics. 2007; 5: 79-94Crossref PubMed Scopus (267) Google Scholar There are additional difficulties correlating the findings in animals with humans. Neurotoxicity is most reliably replicated in animal experiments involving relatively large doses of anesthetic agents per body weight given for a prolonged duration (>4 hours) or in repeated doses to animals that are not undergoing a surgical stress and not as carefully monitored as human babies.11Jevtovic-Todorovic V. Hartman R.E. Izumi Y. et al.Early exposure to common anesthetic agents causes widespread neurodegeneration in the developing rat brain and persistent learning deficits.J Neurosci. 2003; 23: 876-882Crossref PubMed Google Scholar, 18Hayashi H. Dikkes P. Soriano S.G. Repeated administration of ketamine may lead to neuronal degeneration in the developing rat brain.Paediatr Anaesth. 2002; 12: 770-774Crossref PubMed Scopus (170) Google Scholar Surgical stress has been found to ameliorate but not eliminate the apoptotic response to general anesthesia in animal models.19Anand K.J. Garg S. Rovnaghi C.R. Narsinghani U. Bhutta A.T. Hall R.W. Ketamine reduces the cell death following inflammatory pain in newborn rat brain.Pediatr Res. 2007; 62: 283-290Crossref PubMed Scopus (175) Google Scholar In animal models, xenon and dexmedetomidine, which are general anesthetic adjunctive agents, have been found to ameliorate neuroapoptosis, and estradiol, lithium, melatonin, l-carnitine, erythropoietin, and bumetanide have been found to increase prosurvival proteins within the cell cytosol leading to less neuronal cell death.20Edwards D.A. Shah H.P. Cao W. Gravenstein N. Seubert C.N. Martynyuk A.E. Bumetanide alleviates epileptogenic and neurotoxic effects of sevoflurane in neonatal rat brain.Anesthesiology. 2010; 112: 567-575Crossref PubMed Scopus (127) Google Scholar, 21Ma D. Williamson P. Januszewski A. et al.Xenon mitigates isoflurane-induced neuronal apoptosis in the developing rodent brain.Anesthesiology. 2007; 106: 746-753Crossref PubMed Scopus (244) Google Scholar, 22Sanders R.D. Xu J. Shu Y. et al.Dexmedetomidine attenuates isoflurane-induced neurocognitive impairment in neonatal rats.Anesthesiology. 2009; 110: 1077-1085Crossref PubMed Scopus (381) Google Scholar, 23Asimiadou S. Bittigau P. Felderhoff-Mueser U. et al.Protection with estradiol in developmental models of apoptotic neurodegeneration.Ann Neurol. 2005; 58: 266-276Crossref PubMed Scopus (68) Google Scholar, 24Straiko M.M. Young C. Cattano D. et al.Lithium protects against anesthesia-induced developmental neuroapoptosis.Anesthesiology. 2009; 110: 862-868Crossref PubMed Scopus (131) Google Scholar, 25Yon J.H. Carter L.B. Reiter R.J. Jevtovic-Todorovic V. Melatonin reduces the severity of anesthesia-induced apoptotic neurodegeneration in the developing rat brain.Neurobiol Dis. 2006; 21: 522-530Crossref PubMed Scopus (178) Google Scholar, 26Wang C. Sadovova N. Ali H.K. et al.L-carnitine protects neurons from 1-methyl-4-phenylpyridinium-induced neuronal apoptosis in rat forebrain culture.Neuroscience. 2007; 144: 46-55Crossref PubMed Scopus (45) Google Scholar Human trials are underway to examine the efficacy of bumetamide in decreasing the neurologic deficits associated with premature birth in humans. There are several human epidemiologic studies that have linked general anesthetic exposure at a young age with later learning disabilities. Researchers at Mayo Clinic have examined a cohort of more than 5,000 children exposed to anesthesia between 1976 and 1982 before the age of 4 and found there was an association between two or more anesthetics and learning deficits by the age of 18.27Wilder R.T. Flick R.P. Sprung J. et al.Early exposure to anesthesia and learning disabilities in a population-based birth cohort.Anesthesiology. 2009; 110: 796-804Crossref PubMed Scopus (1147) Google Scholar They also found roughly double the cumulative incidence of learning deficits in children exposed to general anesthesia before age 2 using a case–control strategy.28Flick R.P. Katusic S.K. Colligan R.C. et al.Cognitive and behavioral outcomes after early exposure to anesthesia and surgery.Pediatrics. 2011; 128: e1053-e1061Crossref PubMed Scopus (674) Google Scholar Similar findings were reported in studies examining Medicare records in New York State.29DiMaggio C. Sun L.S. Kakavouli A. Byrne M.W. Li G. A retrospective cohort study of the association of anesthesia and hernia repair surgery with behavioral and developmental disorders in young children.J Neurosurg Anesthesiol. 2009; 21: 286-291Crossref PubMed Scopus (425) Google Scholar, 30Dimaggio C. Sun L. Li G. Early childhood exposure to anesthesia and risk of developmental and behavioral disorders in a sibling birth cohort.Anesth Analg. 2011; 113: 1143-1151Crossref PubMed Scopus (427) Google Scholar However, there are also epidemiologic studies that show no evidence of anesthesia-related neurologic deficits in school-aged children. A study of monozygotic twins from the Netherlands revealed that the intellectual attainments were similar between the anesthesia-exposed and nonexposed twin of twin pairs, leading these researchers to conclude that exposure to anesthesia was not a cause of learning deficits.31Bartels M. Althoff R.R. Boomsma D.I. Anesthesia and cognitive performance in children: no evidence for a causal relationship.Twin Res Hum Genet. 2009; 12: 246-253Crossref PubMed Scopus (318) Google Scholar A study from Denmark of more than 2,500 children who underwent inguinal herniorrhaphies as infants found no difference in the ninth grade academic scores compared to a randomly selected sample after adjusting for known confounders.32Hansen T.G. Pedersen J.K. Henneberg S.W. et al.Academic performance in adolescence after inguinal hernia repair in infancy: A nationwide cohort study.Anesthesiology. 2011; 114: 1076-1085Crossref PubMed Scopus (284) Google Scholar In these types of studies, it is very difficult to separate the confounders, that is, the effects of surgery and the morbidities that are associated with the need for surgery from the effects of the exposure to anesthesia. The concern that general anesthesia may be causing apoptotic neuronal death in the immature humans is the preeminent controversy in the pediatric anesthesia community. In response, the Food and Drug Administration and the International Anesthesia Research Society have entered into a public--private partnership called SmartTots to increase the safety of anesthetic drugs by providing research support to investigators in this area. Several ongoing international and national studies are enrolling patients, including the Pediatric Anesthesia Neurodevelopmental Assessment (PANDA) study and the Multi-site Randomized Controlled Trial Comparing Regional and General Anesthesia for Effects on Neurodevelopmental Outcome and Apnea in Infants (GAS) studies. The PANDA study is assembling a cohort of US children who underwent inguinal herniorrhaphy before age 3 and matching them with an unexposed sibling for extensive neurologic and developmental testing. The GAS trial is a multinational randomized controlled trial of preterm and term infants undergoing inguinal herniorrhaphy utilizing either a spinal or a general anesthetic and comparing the neurodevelopmental outcomes of each cohort at ages 2 and 5. The first neurologic outcome results of this prospective randomized equivalence trial should be available in 2014 and should help answer the question of most interest to pediatric ophthalmologists, namely, whether general anesthesia given to infants for procedures that last less than 2 hours is safe. In general, the population of children undergoing pediatric ophthalmological procedures is quite healthy. The procedures are of limited duration and are most commonly done in day surgical units and last from 10 minutes for a blocked tear duct to less than 2 hours even for complex bilateral strabismus surgery. It is important to underscore that not doing the procedures is definitively linked to abnormal neurologic development, particularly in the case of strabismus and cataract surgery. Although several recent epidemiologic studies suggest an association between anesthesia exposure and developmental issues in humans, no study to date has been able to demonstrate a causal link. In addition, several large epidemiologic studies show no association between anesthesia and developmental issues; several others show only an association between prolonged or multiple general anesthetics during early childhood and later developmental issues. Thus, the available epidemiologic data are insufficient to support or refute the contention that general anesthesia causes abnormal neurologic development in humans. Practitioners should reassure their patients and their families that this is an area of ongoing research within the pediatric anesthesia community. The research priorities are the first to determine whether general anesthesia, in fact, does affect human growth and development and, if there is an effect, which anesthetics have the least effect. At this point, the findings of the Food and Drug Administration Anesthesia and Life Support Drugs Advisory Committee in 2007 are still valid: “There are not adequate data to extrapolate the animal findings to humans” and “well-understood risks of anesthesia (respiratory and hemodynamic morbidity) continue to be the overwhelming considerations in designing an anesthetic, and the understood risks of delaying surgery are the primary reasons to determine the timing.”33Anesthetic and Life Support Drugs Advisory Committee. Meeting of March 29, 2007. Available at http://www.fda.gov/ohrms/dockets/ac/07/transcripts/2007-4285t1.pdf.Google Scholar" @default.
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