Impact of Hyperoxia and Hypocapnia on Neurological Outcomes in Patients with Aneurysmal Subarachnoid Hemorrhage: A Retrospective Study

Li, Kin Chio; Tam, Catherine Wing Yan; Shum, Hoi‐Ping; Yan, Wing Wa

doi:10.1155/2019/7584573

Cited by 9 publications

(15 citation statements)

References 28 publications

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“…Hyperoxia effects on cancer biology were explored following multiple pathways, using both in vitro cancer cell cultures and in vivo tumoral animal models. Experimental data support clinical evidences demonstrating that hyperoxia, mainly if prolonged, can induce lung injury and cerebral damage [ 56 , 57 , 58 , 59 , 60 , 61 , 62 ], and this can be counteracted by down-modulation of Akt [ 63 ] or by low-dose vitamin D [ 64 ] or aspirin [ 65 ]. Moreover, hyperoxia diminishes protein synthesis [ 66 ], and high levels of reactive oxygen species trigger expression of several microRNAs in cardiac and pulmonary diseases, as recently reviewed [ 67 , 68 , 69 ].…”

Section: Potential Molecular Mechanisms Exploring Hyperoxia Effects On Cancer Progressionsupporting

confidence: 58%

Exploring Hyperoxia Effects in Cancer—From Perioperative Clinical Data to Potential Molecular Mechanisms

Ristescu

Tiron

et al. 2021

Biomedicines

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Increased inspiratory oxygen concentration is constantly used during the perioperative period of cancer patients to prevent the potential development of hypoxemia and to provide an adequate oxygen transport to the organs, tissues and cells. Although the primary tumours are surgically removed, the effects of perioperative hyperoxia exposure on distal micro-metastases and on circulating cancer cells can potentially play a role in cancer progression or recurrence. In clinical trials, hyperoxia seems to increase the rate of postoperative complications and, by delaying postoperative recovery, it can alter the return to intended oncological treatment. The effects of supplemental oxygen on the long-term mortality of surgical cancer patients offer, at this point, conflicting results. In experimental studies, hyperoxia effects on cancer biology were explored following multiple pathways. In cancer cell cultures and animal models, hyperoxia increases the production of reactive oxygen species (ROS) and increases the oxidative stress. These can be followed by the induction of the expression of Brain-derived neurotrophic factor (BDNF) and other molecules involved in angiogenesis and by the promotion of various degrees of epithelial mesenchymal transition (EMT).

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Section: Potential Molecular Mechanisms Exploring Hyperoxia Effects On Cancer Progressionsupporting

confidence: 58%

Exploring Hyperoxia Effects in Cancer—From Perioperative Clinical Data to Potential Molecular Mechanisms

Ristescu

Tiron

et al. 2021

Biomedicines

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“…The period of data collection ranged from 1996 to 2018 and the cohort size of each study ranged from 196 to 936 patients. Included studies evaluated for hyperoxia exposure at the time of ICU admission 11 or in the first 24 hours, 12,14,16,17 72 hours, 13 or 6 days 15 following admission. There was significant heterogeneity in the methodology used to evaluate hyperoxia exposure.…”

Section: Resultsmentioning

confidence: 99%

“…The reported outcome measures included neurological outcome, incidence of vasospasm and/or DCI, and mortality. ESs were reported as odds ratios 11,[13][14][15][16][17] or risk ratios. 12 Included studies defined poor neurological outcome at, or 3 months after, discharge based on modified Rankin Scale scores of 3 or 4 to 6, or Glasgow Outcome Scale scores < 3.…”

Section: Data Extraction and Outcome Definitionsmentioning

confidence: 99%

“…[8][9][10][11] There is growing literature suggesting an association between early hyperoxemia following aSAH with DCI and poor outcomes. [11][12][13][14][15][16][17] Several mechanisms connecting hyperoxemia with poor outcomes following aSAH have been proposed. Supraphysiological levels of oxygen result in production of reactive oxygen species (ROS), leading to oxidative stress and cerebral inflammation, neuronal death, blood-brain barrier breakdown, and reduction in cerebral blood flow.…”

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confidence: 99%

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Effects of hyperoxemia on aneurysmal subarachnoid hemorrhage outcomes: a systematic review and meta-analysis

Ahn

Mastorakos

Sokolowski

et al. 2022

Neurosurgical Focus

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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.

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“…For this reason, critically ill patients with brain injury frequently receive supplemental oxygen with the hope of increasing oxygen supply to the compromised parts of the brain. Oxygen therapy should be carefully titrated, as hyperoxemia has been associated with worse outcomes in some clinical studies of patients with traumatic brain injury (TBI) or cerebrovascular insult and in patients after cardiac arrest (CA) [3][4][5][6]. Possible mechanisms include an increased formation of reactive oxygen species (ROS), alterations to brain metabolic function, hyperoxia-induced vasoconstriction, and damage to non-injured parts of the brain [7,8].…”

Section: Introductionmentioning

confidence: 99%

The Association Between Arterial Oxygen Level and Outcome in Neurocritically Ill Patients is not Affected by Blood Pressure

et al. 2021

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Background In neurocritically ill patients, one early mechanism behind secondary brain injury is low systemic blood pressure resulting in inadequate cerebral perfusion and consequent hypoxia. Intuitively, higher partial pressures of arterial oxygen (PaO2) could be protective in case of inadequate cerebral circulation related to hemodynamic instability. Study purpose We examined whether the association between PaO2 and mortality is different in patients with low compared to normal and high mean arterial pressure (MAP) in patients after various types of brain injury. Methods We screened the Finnish Intensive Care Consortium database for mechanically ventilated adult (≥ 18) brain injury patients treated in several tertiary intensive care units (ICUs) between 2003 and 2013. Admission diagnoses included traumatic brain injury, cardiac arrest, subarachnoid and intracranial hemorrhage, and acute ischemic stroke. The primary exposures of interest were PaO2 (recorded in connection with the lowest measured PaO2/fraction of inspired oxygen ratio) and the lowest MAP, recorded during the first 24 h in the ICU. PaO2 was grouped as follows: hypoxemia (< 8.2 kPa, the lowest 10th percentile), normoxemia (8.2–18.3 kPa), and hyperoxemia (> 18.3 kPa, the highest 10th percentile), and MAP was divided into equally sized tertiles (< 60, 60–68, and > 68 mmHg). The primary outcome was 1-year mortality. We tested the association between hyperoxemia, MAP, and mortality with a multivariable logistic regression model, including the PaO2, MAP, and interaction of PaO2*MAP, adjusting for age, admission diagnosis, premorbid physical performance, vasoactive use, intracranial pressure monitoring use, and disease severity. The relationship between predicted 1-year mortality and PaO2 was visualized with locally weighted scatterplot smoothing curves (Loess) for different MAP levels. Results From a total of 8290 patients, 3912 (47%) were dead at 1 year. PaO2 was not an independent predictor of mortality: the odds ratio (OR) for hyperoxemia was 1.16 (95% CI 0.85–1.59) and for hypoxemia 1.24 (95% CI 0.96–1.61) compared to normoxemia. Higher MAP predicted lower mortality: OR for MAP 60–68 mmHg was 0.73 (95% CI 0.64–0.84) and for MAP > 68 mmHg 0.80 (95% CI 0.69–0.92) compared to MAP < 60 mmHg. The interaction term PaO2*MAP was nonsignificant. In Loess visualization, the relationship between PaO2 and predicted mortality appeared similar in all MAP tertiles. Conclusions During the first 24 h of ICU treatment in mechanically ventilated brain injured patients, the association between PaO2 and mortality was not different in patients with low compared to normal MAP.

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Impact of Hyperoxia and Hypocapnia on Neurological Outcomes in Patients with Aneurysmal Subarachnoid Hemorrhage: A Retrospective Study

Cited by 9 publications

References 28 publications

Exploring Hyperoxia Effects in Cancer—From Perioperative Clinical Data to Potential Molecular Mechanisms

Exploring Hyperoxia Effects in Cancer—From Perioperative Clinical Data to Potential Molecular Mechanisms

Effects of hyperoxemia on aneurysmal subarachnoid hemorrhage outcomes: a systematic review and meta-analysis

The Association Between Arterial Oxygen Level and Outcome in Neurocritically Ill Patients is not Affected by Blood Pressure

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