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http://hdl.handle.net/1942/14964
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DC Field | Value | Language |
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dc.contributor.author | MEEX, Ingrid | - |
dc.contributor.author | DENS, Jo | - |
dc.contributor.author | JANS, Frank | - |
dc.contributor.author | DE DEYNE, Cathy | - |
dc.date.accessioned | 2013-04-04T12:41:17Z | - |
dc.date.available | 2013-04-04T12:41:17Z | - |
dc.date.issued | 2012 | - |
dc.identifier.citation | EUROPEAN JOURNAL OF ANAESTHESIOLOGY, 29 (Supplement 49 (A30)), p. S9-S9 | - |
dc.identifier.issn | 0265-0215 | - |
dc.identifier.uri | http://hdl.handle.net/1942/14964 | - |
dc.description.abstract | Background: 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.language.iso | en | - |
dc.title | Non-invasive monitoring rebeals a decrease in cerebral oxygenation during therapeutic hypothermia after cardiac arrest | - |
dc.type | Journal Contribution | - |
dc.identifier.epage | S9 | - |
dc.identifier.issue | Supplement 49 (A30) | - |
dc.identifier.spage | S9 | - |
dc.identifier.volume | 29 | - |
local.bibliographicCitation.jcat | M | - |
local.type.refereed | Refereed | - |
local.type.specified | Meeting Abstract | - |
dc.identifier.doi | 10.1097/01.EJA.0000412476.68676.e4 | - |
item.accessRights | Closed Access | - |
item.fulltext | No Fulltext | - |
item.fullcitation | MEEX, 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. | - |
item.contributor | MEEX, Ingrid | - |
item.contributor | DENS, Jo | - |
item.contributor | JANS, Frank | - |
item.contributor | DE DEYNE, Cathy | - |
crisitem.journal.issn | 0265-0215 | - |
crisitem.journal.eissn | 1365-2346 | - |
Appears in Collections: | Research publications |
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