Jungeun Ahn1, Panagiotis Mastorakos2, Jennifer D Sokolowski2, Ching-Jen Chen3, Ryan Kellogg2, Min S Park2. 1. 1School of Medicine, University of Virginia, Charlottesville, Virginia. 2. 2Department of Neurosurgery, University of Virginia Health System, Charlottesville, Virginia; and. 3. 3Department of Neurosurgery, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania.
Abstract
OBJECTIVE: In recent years, hyperoxemia in the intensive care unit has received attention as potentially contributing to negative outcomes in the setting of cardiac arrest, ischemic stroke, and traumatic brain injury. The authors sought to evaluate whether hyperoxemia contributes to worse outcomes in the setting of aneurysmal subarachnoid hemorrhage (aSAH) and to summarize suggested pathophysiological mechanisms. METHODS: A systematic literature review was conducted without date restrictions on the PubMed and Web of Science databases on September 15, 2021. All studies that assessed the relationship between patients treated for aSAH and hyperoxemia were eligible independent of the criteria used to define hyperoxemia. All nonclinical studies and studies that did not report outcome data specific to patients with aSAH were excluded. A total of 102 records were found and screened, resulting in assessment of 10 full-text studies, of which 7 met eligibility criteria. Risk of bias was assessed using the Downs and Black checklist. A meta-analysis on the pooled 2602 patients was performed, and forest plots were constructed. Additionally, a review of the literature was performed to summarize available data regarding the pathophysiology of hyperoxemia. RESULTS: The included studies demonstrated an association between hyperoxemia and increased morbidity and mortality following aSAH. The criteria used to determine hyperoxemia varied among studies. Pooling of univariate data showed hyperoxemia to be associated with poor neurological outcome (OR 2.26, 95% CI 1.66-3.07; p < 0.001), delayed cerebral ischemia (DCI) (OR 1.91, 95% CI 1.31-2.78; p < 0.001), and increased incidence of poor neurological outcome or mortality as a combined endpoint (OR 2.36, 95% CI 1.87-2.97; p < 0.001). Pooling of multivariable effect sizes showed the same relationship for poor neurological outcome (OR 1.28, 95% CI 1.07-1.55; p = 0.01) and poor neurological outcome and mortality as a combined endpoint (OR 1.17, 95% CI 1.11-1.23; p < 0.001). Additionally, review of preclinical studies underlined the contribution of oxidative stress due to hyperoxemia to acute secondary brain injury and DCI. CONCLUSIONS: Reported outcomes from the available studies have indicated that hyperoxemia is associated with worse neurological outcome, mortality, and DCI. These findings provide a general guideline toward avoiding hyperoxemia in the acute setting of aSAH. Further studies are needed to determine the optimal ventilation and oxygenation parameters for acute management of this patient population.
OBJECTIVE: In recent years, hyperoxemia in the intensive care unit has received attention as potentially contributing to negative outcomes in the setting of cardiac arrest, ischemic stroke, and traumatic brain injury. The authors sought to evaluate whether hyperoxemia contributes to worse outcomes in the setting of aneurysmal subarachnoid hemorrhage (aSAH) and to summarize suggested pathophysiological mechanisms. METHODS: A systematic literature review was conducted without date restrictions on the PubMed and Web of Science databases on September 15, 2021. All studies that assessed the relationship between patients treated for aSAH and hyperoxemia were eligible independent of the criteria used to define hyperoxemia. All nonclinical studies and studies that did not report outcome data specific to patients with aSAH were excluded. A total of 102 records were found and screened, resulting in assessment of 10 full-text studies, of which 7 met eligibility criteria. Risk of bias was assessed using the Downs and Black checklist. A meta-analysis on the pooled 2602 patients was performed, and forest plots were constructed. Additionally, a review of the literature was performed to summarize available data regarding the pathophysiology of hyperoxemia. RESULTS: The included studies demonstrated an association between hyperoxemia and increased morbidity and mortality following aSAH. The criteria used to determine hyperoxemia varied among studies. Pooling of univariate data showed hyperoxemia to be associated with poor neurological outcome (OR 2.26, 95% CI 1.66-3.07; p < 0.001), delayed cerebral ischemia (DCI) (OR 1.91, 95% CI 1.31-2.78; p < 0.001), and increased incidence of poor neurological outcome or mortality as a combined endpoint (OR 2.36, 95% CI 1.87-2.97; p < 0.001). Pooling of multivariable effect sizes showed the same relationship for poor neurological outcome (OR 1.28, 95% CI 1.07-1.55; p = 0.01) and poor neurological outcome and mortality as a combined endpoint (OR 1.17, 95% CI 1.11-1.23; p < 0.001). Additionally, review of preclinical studies underlined the contribution of oxidative stress due to hyperoxemia to acute secondary brain injury and DCI. CONCLUSIONS: Reported outcomes from the available studies have indicated that hyperoxemia is associated with worse neurological outcome, mortality, and DCI. These findings provide a general guideline toward avoiding hyperoxemia in the acute setting of aSAH. Further studies are needed to determine the optimal ventilation and oxygenation parameters for acute management of this patient population.
Authors: Jörn Grensemann; Marius Marc-Daniel Mader; Manfred Westphal; Stefan Kluge; Patrick Czorlich Journal: Neurocrit Care Date: 2022-06-08 Impact factor: 3.532