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Updated: May 6, 2026
A Thrombotic Stroke Model Based On Transient Cerebral Hypoxia-ischemia
Published on: August 18, 2015
Association between hyperoxia and mortality after stroke: a multicenter cohort study
Fred Rincon1, Joon Kang, Mitchell Maltenfort
11Department of Neurology, Thomas Jefferson University, Philadelphia, PA. 2Division of Critical Care and Neurotrauma, Department of Neurosurgery, Thomas Jefferson University, Philadelphia, PA. 3Division of Biostatistics, Rothman Institute of Thomas Jefferson University, Philadelphia, PA. 4Department of Medicine, Thomas Jefferson University, Philadelphia, PA. 5Division of Cerebrovascular Diseases, Thomas Jefferson University, Philadelphia, PA.
Objective:
To test the hypothesis that hyperoxia was associated with higher in-hospital mortality in ventilated stroke patients admitted to the ICU.
Design:
Retrospective multicenter cohort study.
Setting:
Primary admissions of ventilated stroke patients with acute ischemic stroke, subarachnoid hemorrhage, and intracerebral hemorrhage who had arterial blood gases within 24 hours of admission to the ICU at 84 U.S. ICUs between 2003 and 2008. Patients were divided into three exposure groups: 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 mortality.
Participants:
Two thousand eight hundred ninety-four patients.
Methods:
Patients were divided into three exposure groups: hyperoxia was defined as PaO2 more than or equal to 300 mm Hg (39.99 kPa), hypoxia as any PaO2 less than 60 mm Hg (7.99 kPa) or PaO2/FIO2 ratio less than or equal to 300, and normoxia, not defined as hyperoxia or hypoxia. The primary outcome was in-hospital mortality.
Interventions:
Exposure to hyperoxia.
Results:
Over the 5-year period, we identified 554 ventilated patients with acute ischemic stroke (19%), 936 ventilated patients with subarachnoid hemorrhage (32%), and 1,404 ventilated patients with intracerebral hemorrhage (49%) of whom 1,084 (38%) were normoxic, 1,316 (46%) were hypoxic, and 450 (16%) were hyperoxic. Mortality was higher in the hyperoxia group as compared with normoxia (crude odds ratio 1.7 [95% CI 1.3-2.1]; p < 0.0001) and hypoxia groups (crude odds ratio, 1.3 [95% CI, 1.1-1.7]; p < 0.01). In a multivariable analysis adjusted for admission diagnosis, other potential confounders, the probability of being exposed to hyperoxia, and hospital-specific effects, exposure to hyperoxia was independently associated with in-hospital mortality (adjusted odds ratio, 1.2 [95% CI, 1.04-1.5]).
Conclusion:
In ventilated stroke patients admitted to the ICU, arterial hyperoxia was independently associated with in-hospital death as compared with either normoxia or hypoxia. These data underscore the need for studies of controlled reoxygenation in ventilated critically ill stroke populations. In the absence of results from clinical trials, unnecessary oxygen delivery should be avoided in ventilated stroke patients.
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