Fred Rincon1, Joon Kang2, Matthew Vibbert1, Jacqueline Urtecho1, M Kamran Athar3, Jack Jallo4. 1. Department of Neurology, Divisions of Critical Care and Neurotrauma, Philadelphia, Pennsylvania, USA Department of Neurology Neurosurgery, Divisions of Critical Care and Neurotrauma, Philadelphia, Pennsylvania, USA. 2. Department of Neurology, Divisions of Critical Care and Neurotrauma, Philadelphia, Pennsylvania, USA. 3. Department of Neurology Neurosurgery, Divisions of Critical Care and Neurotrauma, Philadelphia, Pennsylvania, USA Department of Neurology Medicine, Philadelphia, Pennsylvania, USA. 4. Department of Neurology Neurosurgery, Divisions of Critical Care and Neurotrauma, Philadelphia, Pennsylvania, USA.
Abstract
OBJECTIVE: In this retrospective multi-centre cohort study, we tested the hypothesis that hyperoxia was not associated with higher in-hospital case fatality in ventilated traumatic brain injury (TBI) patients admitted to the intensive care unit (ICU). METHODS: Admissions of ventilated TBI patients who had arterial blood gases within 24 h of admission to the ICU at 61 US hospitals between 2003 and 2008 were identified. Hyperoxia was defined as PaO2 ≥300 mm Hg (39.99 kPa), hypoxia as any PaO2 <60 mm Hg (7.99 kPa) or PaO2/FiO2 ratio ≤300 and normoxia, not defined as hyperoxia or hypoxia. The primary outcome was in-hospital case fatality. RESULTS: Over the 5-year period, we identified 1212 ventilated TBI patients, of whom 403 (33%) were normoxic, 553 (46%) were hypoxic and 256 (21%) were hyperoxic. The case-fatality was higher in the hypoxia group (224/553 [41%], crude OR 2.3, 95% CI 1.7-3.0, p<.0001) followed by hyperoxia (80/256 [32%], crude OR 1.5, 95% CI 1.1-2.5, p=.01) as compared to normoxia (87/403 [23%]). In a multivariate analysis adjusted for other potential confounders, the probability of being exposed to hyperoxia and hospital-specific characteristics, exposure to hyperoxia was independently associated with higher in-hospital case fatality adjusted OR 1.5, 95% CI 1.02-2.4, p=0.04. CONCLUSIONS: In ventilated TBI patients admitted to the ICU, arterial hyperoxia was independently associated with higher in-hospital case fatality. In the absence of results from clinical trials, unnecessary oxygen delivery should be avoided in critically ill ventilated TBI patients. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.
OBJECTIVE: In this retrospective multi-centre cohort study, we tested the hypothesis that hyperoxia was not associated with higher in-hospital case fatality in ventilated traumatic brain injury (TBI) patients admitted to the intensive care unit (ICU). METHODS: Admissions of ventilated TBIpatients who had arterial blood gases within 24 h of admission to the ICU at 61 US hospitals between 2003 and 2008 were identified. Hyperoxia was defined as PaO2 ≥300 mm Hg (39.99 kPa), hypoxia as any PaO2 <60 mm Hg (7.99 kPa) or PaO2/FiO2 ratio ≤300 and normoxia, not defined as hyperoxia or hypoxia. The primary outcome was in-hospital case fatality. RESULTS: Over the 5-year period, we identified 1212 ventilated TBIpatients, of whom 403 (33%) were normoxic, 553 (46%) were hypoxic and 256 (21%) were hyperoxic. The case-fatality was higher in the hypoxia group (224/553 [41%], crude OR 2.3, 95% CI 1.7-3.0, p<.0001) followed by hyperoxia (80/256 [32%], crude OR 1.5, 95% CI 1.1-2.5, p=.01) as compared to normoxia (87/403 [23%]). In a multivariate analysis adjusted for other potential confounders, the probability of being exposed to hyperoxia and hospital-specific characteristics, exposure to hyperoxia was independently associated with higher in-hospital case fatality adjusted OR 1.5, 95% CI 1.02-2.4, p=0.04. CONCLUSIONS: In ventilated TBIpatients admitted to the ICU, arterial hyperoxia was independently associated with higher in-hospital case fatality. In the absence of results from clinical trials, unnecessary oxygen delivery should be avoided in critically ill ventilated TBIpatients. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.
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