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dc.contributor.authorMEEX, Ingrid-
dc.contributor.authorDENS, Jo-
dc.contributor.authorJANS, Frank-
dc.contributor.authorDE DEYNE, Cathy-
dc.identifier.citationEUROPEAN JOURNAL OF ANAESTHESIOLOGY, 29 (Supplement 49 (A30)), p. S9-S9-
dc.description.abstractBackground: Therapeutic hypothermia (TH) improves both survival and neurological outcome after cardiac arrest (CA). Near-infrared spectroscopy provides a continuous monitoring of absolute cerebral tissue oxygen saturation (SctO2). In this study, SctO2 was measured during the first 36 hours after CA. Methods: After IRB approval, data were collected from 23 pts. Cold saline (30 ml/kg) was administered as soon as possible after hospital admission. TH was induced by endovascular or surface cooling and maintained for 24 hours. All pts were sedated (propofol/remifentanil) for duration of hypothermia. Pts were monitored during induction, maintenance and recovery of TH. Results: Of 23 pts, 11 pts did not survive until hospital discharge due to post-ischemic brain damage. Twelve pts survived until hospital discharge (8 without neurological impairment). Temperature at admission was 34,6[degrees]C (+/- 0.5[degrees]C). Pts reached the target temperature of 33[degrees]C, 4 hours after induction of TH. Two pts died during maintenance of TH due to hemodynamic shock. In all patients, SctO2-values started above 65%. Two and a half hours after induction of TH, SctO2 decreased with 9% (+/- 3%). The decrease in SctO2 during induction of TH was not associated with a major change in hemodynamic parameters, nor with a major change in systemic oxygenation. In pts who survived until hospital discharge, SctO2 returned to baseline values 3,5 hours after induction of TH, before the target temperature of 33[degrees]C was reached. In pts who did not survived the hospital stay, SctO2 remained lower than baseline values when target temperature was reached. In these non-survivors, SctO2 only returned to baseline values during maintenance of TH. During rewarming (0,3[degrees]C/h) no significant changes in SctO2 were observed. Conclusion: Therapeutic hypothermia after cardiac arrest induced a decrease in SctO2, with a difference in oxygenation between hospital survivors and non-survivors.-
dc.titleNon-invasive monitoring rebeals a decrease in cerebral oxygenation during therapeutic hypothermia after cardiac arrest-
dc.typeJournal Contribution-
dc.identifier.issueSupplement 49 (A30)-
local.type.specifiedMeeting Abstract-
item.fulltextNo Fulltext-
item.accessRightsClosed Access-
item.contributorDE DEYNE, Cathy-
item.contributorDENS, Jo-
item.contributorJANS, Frank-
item.contributorMEEX, Ingrid-
item.fullcitationMEEX, Ingrid; DENS, Jo; JANS, Frank & DE DEYNE, Cathy (2012) Non-invasive monitoring rebeals a decrease in cerebral oxygenation during therapeutic hypothermia after cardiac arrest. In: EUROPEAN JOURNAL OF ANAESTHESIOLOGY, 29 (Supplement 49 (A30)), p. S9-S9.-
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