Commentary: Machine Learning-Driven Metabolomic Evaluation of Cerebrospinal Fluid: Insights Into Poor Outcomes After Aneurysmal Subarachnoid Hemorrhage

Wipplinger, Christoph; Griessenauer, Christoph J.

doi:10.1093/neuros/nyab033

Cited by 1 publication

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References 24 publications

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“…While large vessel vasospasm is a well-studied risk factor for DCI [22], more recent studies have suggested that a considerable number of patients develop DCI without vasospasm [2,3,23]. Possible underlying pathomechanisms independent of large vessel vasospasm that have been proposed include microthromboembolisms, microvasospasms, inflammation, neurovascular mismatch and cortical spreading depolarization [1,4,[24][25][26][27].…”

Section: Risk Factors For DCImentioning

confidence: 99%

Investigating the relationship between high-dose norepinephrine administration and the incidence of delayed cerebral infarction in patients with aneurysmal subarachnoid hemorrhage: A single-center retrospective evaluation

et al. 2023

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Background One of the longest-standing treatments to prevent delayed cerebral infarction (DCI) in patients with aneurysmal subarachnoid hemorrhage (aSAH) remains raising the blood pressure to a certain level of mean arterial pressure. This may require high doses of norepinephrine, which has been associated with severe end organ damage. With this study, we aimed to investigate the effects of norepinephrine on the incidence of DCI in a clinical setting. Methods We conducted a retrospective evaluation of patients with aSAH admitted to our institution between November 2018 and March 2021. Potential risk factors for DCI were analyzed and significant predictors were assessed by means of a logistic regression analysis to account for potential confounders. Results In this study, 104 patients were included. Hereof, 39 (38%) showed radiologic signs of DCI between day three and 14 post-intervention. These patients had more frequent vasospasms (n = 37 vs. 30, p = 0.022), a higher Hunt & Hess score (3 ± 2 vs. 2 ± 1, p = 0.004), a lower initial Glasgow Coma Scale score (9 ± 5 vs. 12 ± 4, p = 0.003) and received a higher median norepinephrine dose (20,356μg vs. 6,508μg, p < 0.001). A logistic regression analysis revealed that only high-dose norepinephrine administration (OR 2.84, CI 1.56–7.8) and vasospasm (OR 3.07, CI 1.2–7.84) appeared to be significant independent risk factors for DCI. Conclusion Our results indicate a significant association between higher dose norepinephrine administration and the occurrence of DCI. Future research including greater sample sizes and a prospective setting will be necessary to further investigate the relationship.

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