Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/23804
Title: Functional Outcomes in Patients Admitted to the Intensive Care Unit with Traumatic Brain Injury and Exposed to Hyperoxia: A Retrospective Multicentre Cohort Study.
Austin Authors: Weeden, M;Bailey, M;Gabbe, B;Pilcher, D;Bellomo, Rinaldo ;Udy, A
Affiliation: Australian and New Zealand Intensive Care Research Centre, School of Public Health and Preventive Medicine, Monash University, 553 St Kilda Road, Melbourne, VIC, 3004, Australia
Victorian State Trauma Registry, Department of Epidemiology and Preventive Medicine, Monash University, 553 St Kilda Road, Melbourne, VIC, 3004, Australia
Australian and New Zealand Intensive Care Society Centre for Outcome and Resource Evaluation, 10 Levers Terrace, Melbourne, VIC, 3053, Australia
Department of Intensive Care and Hyperbaric Medicine, The Alfred, 55 Commercial Road, Melbourne, VIC, 3004, Australia
Intensive Care
Issue Date: Apr-2021
Date: 2020-07-06
Publication information: Neurocritical Care 2021; 34(2): 441-448
Abstract: Supplemental oxygen administration to critically ill patients is ubiquitous in the intensive care unit (ICU). Uncertainty persists as to whether hyperoxia is benign in patients with traumatic brain injury (TBI), particularly in regard to their long-term functional neurological outcomes. We conducted a retrospective multicenter cohort study of invasively ventilated patients with TBI admitted to the ICU. A database linkage between the Australian and New Zealand Intensive Care Society Adult Patient Database (ANZICS-APD) and the Victorian State Trauma Registry (VSTR) was utilized. The primary exposure variable was minimum acute physiology and chronic health evaluation (APACHE) III PaO2 in the first 24 h of ICU. We defined hypoxia as PaO2 < 60 mmHg, normoxia as 60-299 mmHg, and hyperoxia as ≥ 300 mmHg. The primary outcome was a Glasgow Outcome Scale-Extended (GOSE) < 5 at 6 months while secondary outcomes included 12 and 24 months GOSE and mortality at each of these timepoints. Additional sensitivity analyses were undertaken in the following subgroups: isolated head injury, patients with operative intervention, head injury severity, and PaO2 either subcategorized by increments of 60 mmHg or treated as a continuous variable. A total of 3699 patients met the inclusion criteria. The mean age was 42.8 years, 77.7% were male and the mean acute physiology and chronic health evaluation (APACHE) III score was 60.1 (26.3). 2842 patients experienced normoxia, and 783 hyperoxia. The primary outcome occurred in 1470 (47.1%) of patients overall with 1123 (47.1%) from the normoxia group and 312 (45.9%) from the hyperoxia group-odds ratio 0.99 (0.78-1.25). No significant differences in outcomes between groups at 6, 12, and 24 months were observed. Sensitivity analyses did not identify subgroups that were adversely affected by exposure to hyperoxia. No associations were observed between hyperoxia in ICU during the first 24 h and adverse neurological outcome at 6 months in ventilated TBI patients.
URI: https://ahro.austin.org.au/austinjspui/handle/1/23804
DOI: 10.1007/s12028-020-01033-y
ORCID: 0000-0002-0259-8320
0000-0002-1650-8939
Journal: Neurocritical Care
PubMed URL: 32632905
Type: Journal Article
Subjects: Critical care
Functional neurological outcome
Glasgow Outcome Score-Extended
Hyperoxia
Oxygen toxicity
Traumatic brain injury
Appears in Collections:Journal articles

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