Please use this identifier to cite or link to this item: http://hdl.handle.net/1942/14925
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dc.contributor.authorMEEX, Ingrid-
dc.contributor.authorDENS, Jo-
dc.contributor.authorJANS, Frank-
dc.contributor.authorDE DEYNE, Cathy-
dc.date.accessioned2013-04-03T12:46:34Z-
dc.date.available2013-04-03T12:46:34Z-
dc.date.issued2012-
dc.identifier.citationEUROPEAN JOURNAL OF ANAESTHESIOLOGY, 29 (Supplement 49 (A28)), p. S8-S8-
dc.identifier.issn0265-0215-
dc.identifier.urihttp://hdl.handle.net/1942/14925-
dc.description.abstractBackground: Near-infrared spectroscopy (NIRS) monitors the absolute cerebral tissue oxygen saturation (SctO2). Using four laser wavelengths, absolute determination of oxygenated and deoxygenated hemoglobin in the cerebral microvasculature is provided. Validated by correlation between SctO2 and jugular bulb saturation, threshold for cerebral ischemia is estimated at SctO2-values of 55%. In this study, SctO2 was measured during the first 24 hours after cardiac arrest (CA). Methods: After IRB approval, 23 patients were monitored during the first 24 hours after cardiac arrest (until recovery of therapeutic hypothermia (TH). Cold saline (30 ml/kg) was administered as soon as possible after hospital admission. TH (33[degrees]C) was induced by endovascular or surface cooling. All patients were sedated (propofol/remifentanil) for the duration of TH. SctO2-monitoring was applied before start of TH. Results: Of the 23 patients, 12 (52%) patients survived. Eight of these survivors were discharged without any neurological deficit (CPC1). Two (9%) patients died within the first day after admission due to hemodynamic shock. Nine (39%) patients died as a consequence of post-ischemic brain damage. Values for cerebral oxygenation in non-survivors started at 66% (+/- 7). Within three hours, SctO2 gradually declined to 55% (+/- 4) and remained below this critical value for cerebral ischemia for one hour. Thereafter, SctO2 started to increase to reach baseline values at 12 hours after start of monitoring. The decrease in SctO2 was not correlated with a change in hemodynamic parameters or systemic oxygenation. Patients who survived the hospital stay, started at SctO2 values of 68% (+/- 4). SctO2 decreased to 59% (+/- 5) within two hours, but increased again to baseline values within four hours after the start of monitoring. In the following hours, SctO2 further increased up to 70% (+/- 3). Conclusion: Starting SctO2 values were not different between survivors and non-survivors. However, SctO2-values decreased below the critical limit of 55% in non-survivors.-
dc.language.isoen-
dc.titleCan cerebral oxygenation after cardiac arrest be correlated to outcome?-
dc.typeJournal Contribution-
dc.identifier.epageS8-
dc.identifier.issueSupplement 49 (A28)-
dc.identifier.spageS8-
dc.identifier.volume29-
local.bibliographicCitation.jcatM-
local.type.refereedRefereed-
local.type.specifiedMeeting Abstract-
dc.identifier.doi10.1097/01.EJA.0000412474.61052.9d-
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) Can cerebral oxygenation after cardiac arrest be correlated to outcome?. In: EUROPEAN JOURNAL OF ANAESTHESIOLOGY, 29 (Supplement 49 (A28)), p. S8-S8.-
crisitem.journal.issn0265-0215-
crisitem.journal.eissn1365-2346-
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