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      Hypothermia for neuroprotection in children after cardiopulmonary arrest

      1 , 1 , 2 , 3 , 4 , 5 , 1
      Cochrane Anaesthesia, Critical and Emergency Care Group
      Cochrane Database of Systematic Reviews
      Wiley

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          Abstract

          Cardiopulmonary arrest in paediatric patients often results in death or survival with severe brain injury. Therapeutic hypothermia, lowering of the core body temperature to 32 °C to 34 °C, may reduce injury to the brain in the period after the circulation has been restored. This therapy has been effective in neonates with hypoxic ischaemic encephalopathy and adults after witnessed ventricular fibrillation cardiopulmonary arrest. The effect of therapeutic hypothermia after cardiopulmonary arrest in paediatric patients is unknown. To assess the clinical effectiveness of therapeutic hypothermia after paediatric cardiopulmonary arrest. We searched the Cochrane Anaesthesia Review Group Specialized Register; Cochrane Central Register of Controlled Trials (CENTRAL) ( The Cochrane Library 2011, Issue 11); Ovid MEDLINE (1966 to December 2011); Ovid EMBASE (1980 to December 2011); Ovid CINAHL (1982 to December 2011); Ovid BIOSIS (1923 to December 2011); and Web of Science (1945 to December 2011). We searched the trials registry databases for ongoing trials. We also contacted international experts in therapeutic hypothermia and paediatric critical care to locate further published and unpublished studies. We planned to include randomized and quasi‐randomized controlled trials comparing therapeutic hypothermia with normothermia or standard care in children, aged 24 hours to 18 years, after paediatric cardiopulmonary arrest. Two authors independently assessed articles for inclusion. We found no studies that satisfied the inclusion criteria. We found four on‐going randomized controlled trials which may be available for analysis in the future. We excluded 18 non‐randomized studies. Of these 18 non‐randomized studies, three compared therapeutic hypothermia with standard therapy and demonstrated no difference in mortality or the proportion of children with a good neurological outcome; a narrative report was presented.   Based on this review, we are unable to make any recommendations for clinical practice. Randomized controlled trials are needed and the results of on‐going trials will be assessed when available. Therapeutic hypothermia as a neuroprotective therapy after cardiopulmonary arrest in children Cardiopulmonary arrest in children is uncommon however the numbers of children who survive are very low. Resulting brain injury in the survivors can be devastating for the child and family. Cooling the patient to a temperature of 32 °C to 34 °C, which is 3 °C to 4 °C below normal (therapeutic hypothermia), has previously been found to improve survival and reduce brain injury in newborn infants who were deprived of oxygen during birth, and also in adults following cardiopulmonary arrest. The causes of cardiopulmonary arrest are different in children than in adults, and asphyxia at birth is also different, so the effect of therapeutic hypothermia on the proportion of children who survive or who have brain injury is unclear. We therefore conducted a Cochrane systematic review of the literature, searching medical databases (CENTRAL, MEDLINE, EMBASE) until December 2011 and contacting international experts for high quality published and unpublished evidence. Our searches failed to find any randomized controlled studies that met our inclusion criteria. However, we found four on‐going trials which, when completed, may contribute to our review. At present there is no evidence from randomized controlled trials to support or refute the use of therapeutic hypothermia within a few hours after return of spontaneous blood flow following cardiopulmonary arrest in children. International resuscitation guidelines currently recommend that doctors consider using the therapy in infants and children although more research is needed to be sure this is the correct recommendation with the lack of treatment options other than supportive care in an intensive care unit that are available.

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          Most cited references46

          • Record: found
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          First documented rhythm and clinical outcome from in-hospital cardiac arrest among children and adults.

          Cardiac arrests in adults are often due to ventricular fibrillation (VF) or pulseless ventricular tachycardia (VT), which are associated with better outcomes than asystole or pulseless electrical activity (PEA). Cardiac arrests in children are typically asystole or PEA. To test the hypothesis that children have relatively fewer in-hospital cardiac arrests associated with VF or pulseless VT compared with adults and, therefore, worse survival outcomes. A prospective observational study from a multicenter registry (National Registry of Cardiopulmonary Resuscitation) of cardiac arrests in 253 US and Canadian hospitals between January 1, 2000, and March 30, 2004. A total of 36,902 adults (> or =18 years) and 880 children (<18 years) with pulseless cardiac arrests requiring chest compressions, defibrillation, or both were assessed. Cardiac arrests occurring in the delivery department, neonatal intensive care unit, and in the out-of-hospital setting were excluded. Survival to hospital discharge. The rate of survival to hospital discharge following pulseless cardiac arrest was higher in children than adults (27% [236/880] vs 18% [6485/36,902]; adjusted odds ratio [OR], 2.29; 95% confidence interval [CI], 1.95-2.68). Of these survivors, 65% (154/236) of children and 73% (4737/6485) of adults had good neurological outcome. The prevalence of VF or pulseless VT as the first documented pulseless rhythm was 14% (120/880) in children and 23% (8361/36,902) in adults (OR, 0.54; 95% CI, 0.44-0.65; P<.001). The prevalence of asystole was 40% (350) in children and 35% (13 024) in adults (OR, 1.20; 95% CI, 1.10-1.40; P = .006), whereas the prevalence of PEA was 24% (213) in children and 32% (11,963) in adults (OR, 0.67; 95% CI, 0.57-0.78; P<.001). After adjustment for differences in preexisting conditions, interventions in place at time of arrest, witnessed and/or monitored status, time to defibrillation of VF or pulseless VT, intensive care unit location of arrest, and duration of cardiopulmonary resuscitation, only first documented pulseless arrest rhythm remained significantly associated with differential survival to discharge (24% [135/563] in children vs 11% [2719/24,987] in adults with asystole and PEA; adjusted OR, 2.73; 95% CI, 2.23-3.32). In this multicenter registry of in-hospital cardiac arrest, the first documented pulseless arrest rhythm was typically asystole or PEA in both children and adults. Because of better survival after asystole and PEA, children had better outcomes than adults despite fewer cardiac arrests due to VF or pulseless VT.
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            Assessing the outcome of pediatric intensive care.

            D Fiser (1992)
            To describe the short-term outcome of pediatric intensive care by quantifying overall functional morbidity and cognitive impairment, I developed the Pediatric Overall Performance Category (POPC) and the Pediatric Cerebral Performance Category (PCPC) scales, respectively. A total of 1469 subjects (1539 admissions) were admitted to the pediatric intensive care unit of Arkansas Children's Hospital from July 1989 through December 1990. Patients were assigned baseline POPC and PCPC scores derived from historical information and discharge scores at the time of discharge from the hospital (or from the pediatric intensive care unit for patients with multiple hospitalizations). Delta scores were calculated as the difference between the discharge scores and the baseline scores. The changes in POPC and PCPC scores were associated with several measures of morbidity (length of stay in the pediatric intensive care unit, total hospital charges, and discharge care needs) and with severity of illness (pediatric risk of mortality score) or severity of injury (pediatric trauma score) (p less than 0.0001). Interrater reliability was excellent (r = 0.88 to 0.96; p less than 0.001). The POPC and PCPC scales are apparently reliable and valid tools for assessing the outcome of pediatric intensive care.
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              Small differences in intraischemic brain temperature critically determine the extent of ischemic neuronal injury.

              We have tested whether small intraischemic variations in brain temperature influence the outcome of transient ischemia. To measure brain temperature, a thermocouple probe was placed stereotaxically into the left dorsolateral striatum of rats prior to 20 min of four-vessel occlusion. Rectal temperature was maintained at 36-37 degrees C by a heating lamp, and striatal temperature prior to ischemia was 36 degrees C in all animals. Six animal subgroups were investigated, including rats whose intraischemic striatal brain temperature was not regulated, or was maintained at 33, 34, 36, or 39 degrees C. Postischemic brain temperature was regulated at 36 degrees C, except for one group in which brain temperature was lowered from 36 degrees C to 33 degrees C during the first hour of recirculation. Energy metabolites were measured at the end of the ischemic insult, and histopathological evaluation was carried out at 3 days after ischemia. Intraischemic variations in brain temperature had no significant influence on energy metabolite levels measured at the conclusion of ischemia: Severe depletion of brain ATP, phosphocreatine, glucose, and glycogen and elevation of lactate were observed to a similar degree in all experimental groups. The histopathological consequences of ischemia, however, were markedly influenced by variations in intraischemic brain temperature. In the hippocampus, CA1 neurons were consistently damaged at 36 degrees C, but not at 34 degrees C. Within the dorsolateral striatum, ischemic cell change was present in 100% of the hemispheres at 36 degrees C, but in only 50% at 34 degrees C. Ischemic neurons within the central zone of striatum were not observed in any rats at 34 degrees C, but in all rats at 36 degrees C. In rats whose striatal temperature was not controlled, brain temperature fell from 36 to 30-31 degrees C during the ischemic insult. In this group, no ischemic cell change was seen within striatal areas and was only inconsistently documented within the CA1 hippocampal region. These results demonstrate that (a) rectal temperature unreliably reflects brain temperature during ischemia; (b) despite severe depletion of brain energy metabolites during ischemia at all temperatures, small increments of intraischemic brain temperature markedly accentuate histopathological changes following 3-day survival; and (c) brain temperature must be controlled above 33 degrees C in order to ensure a consistent histopathological outcome. Lowering of the brain temperature by only a few degrees during ischemia confers a marked protective effect.
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                Author and article information

                Journal
                Cochrane Database of Systematic Reviews
                Wiley
                14651858
                February 28 2013
                Affiliations
                [1 ]Birmingham Children's Hospital; Paediatric Intensive Care Unit; Steelhouse Lane Birmingham UK B4 6NH
                [2 ]Birmingham Children's Hospital; Department of Research and Development; Steelhouse Lane Birmingham UK B4 6NH
                [3 ]University of Birmingham; Perioperative, Critical Care and Trauma Trials Group, School of Clinical and Experimental Medicine; Birmingham UK
                [4 ]Barts and the London School of Medicine, Queen Mary, University of London; Centre for Health Sciences; London UK
                [5 ]Warwick Medical School and Heart of England NHS Foundation Trust; Warwick UK
                Article
                10.1002/14651858.CD009442.pub2
                6517232
                23450604
                8acfa14d-4866-4f2d-8ccd-1dafc94dd99f
                © 2013
                History

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